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Name:

News Article Title and Link:

Short Description in Your Own Words:

Scientific Paper Title and Link:

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A long-overlooked weak point in your DNA has just been revealed

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Scientists discovered that the first 100 base pairs of human genes are unusually prone to mutations, especially during the earliest stages of embryonic development. These mosaic mutations often go undetected yet can still be passed on and cause disease. Large-scale genome analyses show that genes tied to cancer and brain function are particularly affected, with natural selection filtering out harmful variants. The study highlights the need to adjust genetic models and rethink how researchers identify disease-relevant mutations.

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Name: Becky Seipelt-Thiemann

News Article: A long-overlooked weak point in your DNA has just been revealed: https://www.sciencedaily.com/releases/2025/12/251202052217.htm

Short Description: Mutations in the first part of genes are more common than we thought - cancer and brain function are highly affected by this.

Scientific Paper: Transcription start sites experience a high influx of heritable variants fueled by early development: https://www.nature.com/articles/s41467-025-66201-0

# data[].attributes.attachment_link.title
A long-overlooked weak point in your DNA has just been revealed

# data[].attributes.attachment_link.description
Scientists discovered that the first 100 base pairs of human genes are unusually prone to mutations, especially during the earliest stages of embryonic development. These mosaic mutations often go undetected yet can still be passed on and cause disease. Large-scale genome analyses show that genes tied to cancer and brain function are particularly affected, with natural selection filtering out harmful variants. The study highlights the need to adjust genetic models and rethink how researchers identify disease-relevant mutations.

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Name: Jaylin Moore

News Article: Why some people age faster. And the 400 genes behind it: https://www.sciencedaily.com/releases/2025/08/250821094516.htm

Short Description: Scientists have discovered 408 genes associated with faster aging, each associated with one of six sub-types of "unhealthy aging" that can be preventatively targeted.

Scientific Paper: Uncovering the multivariate genetic architecture of frailty with genomic structural equation modeling: https://www.nature.com/articles/s41588-025-02269-0

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Why some people age faster. And the 400 genes behind it

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Researchers identified over 400 genes tied to various forms of frailty, offering fresh insight into why people age differently. The study highlights six distinct pathways of unhealthy aging, opening the door to more precise, targeted anti-aging interventions.

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Name: Nichole Stude

Description: Researchers at Stanford Medicine have found that by blocking the 15-PGDH enzyme using an injection of small inhibitor molecules, natural knee cartilage loss from aging and arthritis development decreases.

Link: www.sciencedaily.com/releases/2026/01/260120000333.htm

Article: www.science.org/doi/10.1126/science.adx6649

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Stanford scientists found a way to regrow cartilage and stop arthritis

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Scientists at Stanford Medicine have discovered a treatment that can reverse cartilage loss in aging joints and even prevent arthritis after knee injuries. By blocking a protein linked to aging, the therapy restored healthy, shock-absorbing cartilage in old mice and injured joints, dramatically improving movement and joint function. Human cartilage samples from knee replacement surgeries also began regenerating when exposed to the treatment.

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Name: Kenzie Ray

News Article: The genetic advantage that helps some people stay sharp for life

The genetic advantage that helps some people stay sharp for life | ScienceDaily

Short Description: A new study shows that healthy, cognitively inclined seniors over 80 have a distinct genetic advantage involving a gene related to Alzheimer's.

Scientific paper: Evaluating the association of apolipoprotein E genotype and cognitive resilience in SuperAgers

Evaluating the association of apolipoprotein E genotype and cognitive resilience in SuperAgers - Durant - 2026 - Alzheimer's & Dementia - Wiley Online Library

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The genetic advantage that helps some people stay sharp for life

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A new study reveals that super agers over 80 have a distinct genetic edge. They are much less likely to carry the gene most associated with Alzheimer’s risk, even when compared with other healthy seniors. Researchers also found higher levels of a protective gene variant in this group. Together, the findings help explain why some people age with remarkably youthful minds.

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Name: Eliana Rumberg

News Article: Genetic basis of purring in cats:https://www.sciencedaily.com/releases/2025/05/250529124402.htm

Short Description: House cats are comforting companions and unlike other species of cats they are social and communicate with each other like purring.

Scientific Paper: Association between androgen receptor gene and behavioral traits in cats (Felis catus) https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0324055

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Whether you are lucky enough to have a cat companion or must merely live this experience vicariously through cat videos, Felis catus is a familiar and comforting presence in our daily lives. Unlike most other feline species, cats exhibit sociality, can live in groups, and communicate both with other cats and humans, which is why they have been humans' trusted accomplices for millennia. Despite this intimacy, there is still much that we don't know about our feline friends.

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Name: Blessing Chukwuneke

New Article: Scientists find the missing links between genes and disease: https://www.sciencedaily.com/releases/2025/12/251215084201.htm

Short Description: A detailed genomic road map showing how thousands of genes work together in coordinated networks to influence human disease. Reveals hidden regulatory connections that help explain why certain genetic variants increase disease risk.

Scientific Paper: A comprehensive gene regulatory network map reveals coordinated modules underlying human disease risk:
https://www.nature.com/articles/s41586-025-09909-9

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Scientists have unveiled a powerful new way to map how genes work together to drive disease, offering a long-sought bridge between genetic clues and biological meaning. Credit: Shutterstock

Biomedical scientists are racing to identify the genes that contribute to illness, hoping that these discoveries will lead to treatments that target the right genes and help bring the body back to health.

When one faulty gene is responsible, the path to understanding the problem can be fairly direct. Many conditions, however, are far more complicated. In these cases, multiple genes, sometimes even thousands, play a role, and it becomes much harder to sort out how they connect to the disease.

A new genomic mapping approach could make that challenge easier to tackle. In a Nature study, researchers at Gladstone Institutes and Stanford University used a broad strategy that tests the impact of every gene in a cell, linking diseases and other traits to the underlying genetic systems that shape them. The resulting maps could cut through confusing biology and spotlight the genes most likely to be useful targets for new therapies.

"We can now look across every gene in the genome and get a sense of how each one affects a particular cell type," says Gladstone Senior Investigator Alex Marson, MD, PhD, the Connie and Bob Lurie Director of the Gladstone-UCSF Institute of Genomic Immunology, who co-led the study. "Our goal is to use this information as a map to gain new insights into how certain genes influence specific traits."
Finding the 'Why' Behind Genetic Risk
For years, scientists have relied heavily on "genome-wide association studies," which scan the DNA of thousands of people to find statistical links between genetic differences and traits, including disease risk. These efforts have generated enormous datasets, but turning those signals into clear biological explanations can be difficult, especially for traits influenced by many genes.

"Even with these studies, there remains a huge gap in understanding disease biology on a genetic level," says first author Mineto Ota, MD, PhD. Ota is a postdoctoral scholar in Marson's Gladstone lab, as well as in the lab of Stanford scientist Jonathan Pritchard, PhD. "We understand that many variants are associated with disease; we just don't understand why."

Mineto compares it to having a map with a clear starting point and endpoint, but no routes connecting the two.

"To understand complex traits, we really need to focus on the network," says Pritchard, a professor of Biology and Genetics at Stanford, who co-led the study with Marson. "How do we think about biology when thousands and thousands of genes, with many different functions, are all affecting a trait?"
Combining Cell Experiments With Big Population Data
To dig into that network problem, the researchers pulled information from two databases.

One dataset came from a human leukemia cell line that is commonly used to study red blood cell traits. In earlier work, an MIT researcher who was not involved in this study had switched off each gene in that cell line, one at a time, and tracked how losing that gene changed genetic activity.

Marson's team then paired those results with UK Biobank data, which includes genomic sequences from more than 500,000 people. Ota searched for individuals with genetic mutations that lowered gene function in ways that changed their red blood cells.

Putting the two sources together allowed the researchers to build a detailed map of the gene networks that influence red blood cell traits. The picture that emerged showed a remarkably complex genetic landscape. With this approach, they could see the starting point, the destination, and the intricate set of connections in between.

They also discovered that some genes affect several biological processes at the same time, weakening certain activities while increasing others. One example is SUPT5H, a gene associated with beta thalassemia, a blood disorder that disrupts hemoglobin production and can lead to moderate to severe anemia. The researchers connected SUPT5H to three key blood cell programs: hemoglobin production, cell cycle, and autophagy. They also showed how the gene influences each program, either increasing or reducing gene activity.

"SUPT5H regulates all three main pathways that affect hemoglobin," Pritchard says. "It activates hemoglobin synthesis, slows down the cell cycle, and slows down autophagy, which together have a synergistic effect."
Why This Mapping Method Could Matter for Immunology
Being able to reveal the detailed genetic pathways that control how cells function could reshape both basic biology and drug development.

Although the team identified multiple ways gene networks shape blood cell behavior, the bigger story is the tool itself. The research group, and potentially many other scientists, can now apply the same strategy to other human cell types to uncover the molecular patterns that drive disease.

For the Marson lab, which focuses on T cells and other parts of the immune system, the method could open the door to many more discoveries.

"The genetic burden associated with many autoimmune diseases, immune deficiencies, and allergies are overwhelmingly linked to T cells," Marson says. "We look forward to developing additional detailed maps that will help us really understand the genetic architecture behind these immune-mediated diseases."

The study, "Causal modeling of gene effects from regulators to programs to traits," appears in the December 10, 2025 issue of Nature. Authors include: Mineto Ota, Jeffrey Spence, Tony Zeng, Emma Dann, Nikhil Milind, Alexander Marson, and Jonathan Pritchard. This research was funded by the National Institutes of Health, the Simons Foundation, the Lloyd J. Old STAR Award, the Parker Institute for Cancer Immunotherapy, the Innovative Genomics Institute, the Larry L. Hillblom Foundation, the Northern California JDRF Center of Excellence, the Byers family, K. Jordan, the CRISPR Cures for Cancer Initiative, the Astellas Foundation for Research on Metabolic Disorders, the Chugai Foundation for Innovative Drug Discovery Science, and the EMBO Postdoctoral Fellowship.

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leukemia; allergy; diseases and conditions; workplace health; pharmaceuticals; immune system; human biology; pharmacology

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Scientists find the missing links between genes and disease

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A new genetic mapping strategy reveals how entire networks of genes work together to cause disease, filling in the missing links left by traditional genetic studies. The technique could transform how scientists identify drug targets for complex conditions.

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Name: Laurel Thompson

News Article: Genetic study reveals hidden chapter in human evolution:

https://www.sciencedaily.com/releases/2025/03/250318141412.htm

Short Description: A study shows that modern humans probably resulted from a population mixing event rather than from one lineage. These populations drifted, then later reconnected.

Scientific Paper: A structured coalescent model reveals deep ancestral structure shared by all modern humans:

https://www.nature.com/articles/s41588-025-02117-1

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Genetic study reveals hidden chapter in human evolution

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Modern humans descended from not one, but at least two ancestral populations that drifted apart and later reconnected, long before modern humans spread across the globe.

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Ghost population found hidden in the genome of West African populations

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Ghost population found hidden in the genome of West African populations

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Name: Habibatu Kamara

News Article Title & Link: Ghost population found hidden in the genome of West African populations

https://www.biotechniques.com/computational-biology/expanding-our-search-for-antibiotics-encrypted-biology-ancient-datasets-and-ai/

Brief description: Researchers from the University of California, Los Angeles have found genetic evidence of an unknown, extinct human by analyzing the genomes of modern West African populations. Biologist found that around 8% of the genetic ancestry of four West African populations hail from said ghost hominid, which is distinct from Neanderthals and Denisovans.

Scientific article title and link: Recovering signals of ghost archaic introgression in African populations https://advances.sciencemag.org/content/6/7/eaax5097

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Ghost population found hidden in the genome of West African populations

# data[].attributes.attachment_link.description
Evidence for a previously unknown species of archaic hominin can be found in the genes of modern-day West African populations.

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Chronic gut inflammation and colon cancer

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Chronic gut inflammation and colon cancer

# data[].attributes.body
Name: Hannah Espiritu

News Article: Why chronic gut inflammation can turn into colon cancer: https://www.sciencedaily.com/releases/2026/01/260125083401.htm

Short Description: The inflammatory signal protein, TL1A, associated with irritable bowel disease (IBD) and colorectal cancer was found to activate gut-specific immune cells whose pattern drives tumor growth formation through gene activity and expression changes.

Scientific Paper: Innate lymphoid cells activated by the cytokine TL1A link colitis to emergency granulopoiesis and the recruitment of tumor-promoting neutrophils:

https://www.cell.com/immunity/fulltext/S1074-7613(25)00564-3

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Why chronic gut inflammation can turn into colon cancer

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A newly uncovered immune chain reaction in the gut may explain why people with inflammatory bowel disease face a much higher risk of colorectal cancer. Researchers found that a powerful inflammatory signal flips on specialized gut immune cells, which then call in waves of white blood cells from the bone marrow and rewire them in ways that help tumors grow. This process appears to damage DNA in the gut lining and create a tumor-friendly environment.

# data[].attributes.body
Name: Emily Olson

News Article: Antiviral insights: cyro-EM and optical tweezers reveal more about drug-herpes virus interaction

Illuminating The Inner Workings of Antivirals - BioTechniques

Short Description: A new study shows how new class of antivirals treats HSV infections. These antivirals target the helicase-primase of the virus to prevent the virus's DNA from replicating.

Scientific Paper: Mechanisms of HSV-1 helicase-primase inhibition and replication fork complex assembly

Mechanisms of HSV-1 helicase-primase inhibition and replication fork complex assembly: Cell

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Original story from Harvard Medical School (MA, USA). Cryo-EM images show drugs bound to herpes simplex virus protein at nearly atomic detail, while optical tweezer experiments show how the drug-bound protein behaves in real time.
Harvard Medical School (HMS; MA, USA) researchers have uncovered crucial insights into how an emerging class of antiviral drugs works. The discovery sheds light on an important tool for fighting drug-resistant strains of herpes simplex virus, or HSV, and points to new pathways for treating herpesviruses and other kinds of DNA viruses (those that have DNA as their genetic material and can replicate inside host cells).

Members of a new class of antivirals are being tested in US clinical trials, and one has gained approval in Japan, but how these emerging drugs work is mostly unknown. Researchers used structural biology insights and imaging techniques to explore the biophysical mechanisms at play as the new drugs bind to and inactivate a critical enzyme in the life cycle of HSV.

Co-senior author Jonathan Abraham and his lab focused on revealing the structural details of how the drugs locked to the viral protein, while co-senior author Joseph Loparo's lab worked on capturing real-time details about how the binding process works to block the viral protein.
This article has been republished from the following . Material may have been edited for length and house style. For further information, please contact the cited source. Our press release publishing policy can be accessed .

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Antiviral insights: cryo-EM and optical tweezers reveal more about drug-herpes virus interaction

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Researchers use cryo-EM and optical tweezers to investigate how an antiviral interacts with the herpes simplex virus.

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Name: Ana Alarcon

News Article: A hidden genetic war is unfolding inside your DNA

https://www.sciencedaily.com/releases/2026/01/260125083418.htm

Short Description: The article covers an arms race between depleting chromosome ends and biological mechanisms that try to slow the process.

Scientific Paper: Rapid compensatory evolution within a multiprotein complex preserves telomere integrity

https://www.science.org/doi/10.1126/science.adv0657

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A hidden genetic war is unfolding inside your DNA

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Our genome isn’t as peaceful as it looks—some DNA elements are constantly trying to disrupt it. Scientists studying fruit flies discovered that key proteins protecting chromosome ends must evolve rapidly to counter these internal threats. When these proteins fall out of sync, chromosomes fuse and cells die. The work reveals how essential biological systems survive by constantly reinventing themselves.

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Asthma’s real trigger may be a hidden chemical wildfire—and scientists just found the spark.

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Asthma’s real trigger may be a hidden chemical wildfire—and scientists just found the spark.

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Name: Kamari Hawkins

News Article: Scientists may have been wrong about what causes asthma

https://www.sciencedaily.com/releases/2026/01/260127010147.htm

Short Description: A group of researchers found a high level of “pseudo-leukotrienes,” an inflammation-triggering compound, in individuals with mild to severe asthma. These discoveries have led to potential asthma treatments that could prevent the inflammation rather than blocking the reaction.

Scientific Paper: Radical-induced lipid oxidation produces a torrent of leukotriene-like agonists in severe asthma

https://www.sciencedirect.com/science/article/pii/S0091674925010267?via%3Dihub

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Scientists may have been wrong about what causes asthma

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Asthma may not be driven by the molecules scientists have blamed for decades. Researchers have identified "pseudo leukotrienes," inflammation-triggering compounds formed by uncontrolled free-radical reactions rather than normal enzymes. These molecules were found at much higher levels in people with asthma, closely tracking how severe their symptoms were.

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Name: Eliana Rumberg

News Article: Advancing human genomics with nanopore sequencing: https://www.biotechniques.com/pcr-sequencing/on_advancing-human-genomics-with-nanopore-sequencing/

Short Description: Nanopore sequencing is helping to overcome challenges with short-read sequences and better understand the human genome.

Scientific Paper: https://info.biotechniques.com/hubfs/BTN/2024/Oxford%20Nanopore/Oxford%20Nanopore%20human-genetics-research-white-paper.pdf

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Advancing human genomics with nanopore sequencing

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High-throughput sequencing technologies have revolutionized the field of human genetics, allowing researchers to further our understanding of biological processes and their impact. However, the use of traditional short-read sequencing technologies presents many limitations, including the inability to analyze repeat regions, structural variants, phasing, full-length transcript isoforms, and methylation. This White Paper describes how researchers are […]

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Scientists have found that cancer evolution follows hidden rules shaped by chromosome gains and losses, not random chaos.

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Cancer Evolution                              Joseph Girgis

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Cancer Evolution                              Joseph Girgis

# data[].attributes.body
Name: H. Lee Moffitt

News Article: Scientists just cracked the hidden rules of cancer evolution:

https://www.sciencedaily.com/releases/2026/01/260125083344.htm

Short Description: From recent studies, researchers have enveloped a new concept that tracks thousands of cancer (mutated) cells overtime, showing predictable patterns on how tumors lose and gain entire chromosomes. These major genetic modifications benefit cancer cells through the means of survival advantages, tumor growth, adaptations, and resistants to treatments, offering valuable insight into why cancer cells are so resilient.

Scientific paper: Revealing patterns in how cancer cells gain and lose whole chromosomes and how those changes influence tumor evolution and treatment resistance.

Richard J. Beck, Tao Li, Noemi Andor. ALFA-K: Local adaptive mapping of karyotype fitness landscapes. Nature Communications, 2025; DOI: 10.1038/s41467-025-67750-0

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Regions of crypt destruction and/or inflammatory infiltrates. Scale bar: 200 μm

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AI Cracks Quarter-Century Crohn's Mystery

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AI Cracks Quarter-Century Crohn's Mystery

# data[].attributes.body
Mari Zamora

UC San Diego Researchers employ Artificial Intelligence tools to track 53 genetic markers for aggressive inflammation in Crohn's disease to identify key differences in protein expression and interaction that relate to an exaggerated inflammatory response.

From Science Daily: A 25-year Crohn’s disease mystery finally cracked by AI

From The Journal of Clinical Investigation: Distinct colitis-associated macrophages drive NOD2-dependent bacterial sensing and gut homeostasis

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Genetic Risk of Schizophrenia Affects Males and Females Differently

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Genetic Risk of Schizophrenia Affects Males and Females Differently

# data[].attributes.body
Name: Genesis Morrow

News Article: Genetic risk of schizophrenia affects men and women differently: Genetic risk of schizophrenia affects men and women differently | ScienceDaily

Short Description: A study examined the relationship between moderate subclinical characteristics in the general population and the genetic risk of developing schizophrenia. The study found that these subclinical characteristics are influenced differently in men and women by the hereditary risk of having this condition.

Scientific Paper: Sex-specific association between schizophrenia polygenic risk and subclinical schizophrenia-related traits: Sex-specific association between schizophrenia polygenic risk and subclinical schizophrenia-related traits - ScienceDirect

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Researchers Discover Hidden Genetic Causes of Congenital Heart Disease

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Researchers Discover Hidden Genetic Causes of Congenital Heart Disease

# data[].attributes.body
Name: Emily Olson

Short Description: Researchers discovered 10 new gene pairs leading to congenital heart disease. This study shows the potential for digenic inheritance, when multiple genes work together to cause a disease, which has been previously hard to prove due to type 1 errors and location of genes on the chromosome.

News Article: Researchers Discover Hidden Genetic Causes of Congenital Heart Disease

Scientific Paper: Deciphering the digenic architecture of congenital heart disease using trio exome sequencing data

Deciphering the digenic architecture of congenital heart disease using trio exome sequencing data: The American Journal of Human Genetics

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The Mount Sinai Hospital / Mount Sinai School of Medicine

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Researchers Discover Hidden Genetic Causes of Congenital Heart Disease

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A new approach reveals genetic interactions that contribute to heart defects. Scientists at the Icahn School of Medicine at Mount Sinai, in collaboration with others, have discovered new genetic interactions that may play a role in congenital heart disease (CHD), one of the most common birth defect

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Name: Amber Goins

News Article: Are Identical Twins Really Identical? https://www.the-scientist.com/are-identical-twins-really-identical-73178

Short Description: This article explains that even though identical (monozygotic) twins come from the same fertilized egg and share nearly the same DNA, they are not completely identical. Over time, differences in their environments can cause changes in gene expression through epigenetic mechanisms like DNA methylation and histone modification. These changes can lead to differences in physical traits, disease risk, and overall health.

Scientific Paper: Epigenetic differences arise during the lifetime of monozygotic twins

https://www.pnas.org/doi/full/10.1073/pnas.0500398102

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Despite sharing DNA sequences, monozygotic twins are epigenetically distinct and express different genes, offering a model to better understand diseases.

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Name: Julie Mehany

News Article: Expanding the CRISPR toolbox: new mechanism could push boundaries of gene editing

https://www.biotechniques.com/crispr/expanding-the-crispr-toolbox-new-mechanism-could-push-boundaries-of-gene-editing/

Short Description: An unexpected discovery of the ability to use the CRISPR-Cas system (Cas12a3 specifically mentioned) to target and destroy tRNAs, thus halting the translation of mRNA into its associated protein.

Scientific Paper: RNA-triggered Cas12a3 cleaves tRNA tails to execute bacterial immunity

https://www.nature.com/articles/s41586-025-09852-9

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Expanding the CRISPR toolbox: new mechanism could push boundaries of gene editing

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New CRISPR mechanism could expand the potential applications of the existing CRISPR toolbox.

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Link between P53 inactivation and breast cancer metastasis to the brain

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Link between P53 inactivation and breast cancer metastasis to the brain

# data[].attributes.body
Name: Seamus Koch

News Article: For the first time, a mechanism enabling breast cancer to metastasize to the brain has been deciphered https://medicalxpress.com/news/2026-01-mechanism-enabling-breast-cancer-metastasize.html

Short Description: Breast cancer cells that had the tumor suppressor gene, p53, knocked out were shown to cause brain metastasis. P53's alteration in these cells cause upregulation to SCD1 and Fatty acids, both of which are used during the process of cancer metastasis to the brain.

Scientific Paper: p53 inactivation drives breast cancer metastasis to the brain through SCD1 upregulation and increased fatty acid metabolism https://www.nature.com/articles/s41588-025-02446-1

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Inactivation of p53 drives breast cancer brain metastasis by altering fatty acid metabolism

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Brain metastasis (BM) is a dire prognosis across cancer types. It is largely unknown why some tumors metastasize to the brain whereas others do not. We analyzed genomic and transcriptional data from clinical samples of breast cancer BM (BCBM) and found that nearly all of them carried p53-inactivating genetic alterations through mutations, copy-number loss, or both. Importantly, p53 pathway activity was already perturbed in primary tumors giving rise to BCBM, often by loss of the entire 17p chromosome-arm. This association was recapitulated across other carcinomas. Experimentally, p53 knockout was sufficient to drastically increase BCBM formation and growth in vivo , providing a causal link between p53 inactivation and brain tropism. Mechanistically, p53-deficient BC cells exhibited altered lipid metabolism, particularly increased fatty acid (FA) synthesis and uptake, which are characteristic of brain-metastasizing cancer cells. FA metabolism was further enhanced by astrocytes in a p53-dependent manner, as astrocyte-conditioned medium increased FASN, SCD1, and CD36 expression and activity, and enhanced the survival, proliferation and migration of p53-deficient cancer cells. Consequently, these cells were more sensitive than p53-competent cells to FA synthesis inhibitors, in isogenic cell cultures, in BCBM-derived spheroids, and across dozens of BC cell lines. Lastly, a significant association was observed between p53 inactivation, astrocyte infiltration, and SCD1 expression in clinical human BCBM samples. In summary, our study identifies p53 inactivation as a driver of BCBM and potentially of BM in general; suggests a p53-dependent effect of astrocytes on BC cell behavior; and reveals FA metabolism as an underlying, therapeutically-targetable molecular mechanism. ### Competing Interest Statement R.S.-F. is a Board Director at Teva Pharmaceutical Industries Ltd. and receives unrelated research funding from Merck KGaA. U.B.-D. received unrelated research funding from Novocure Ltd. All other authors have no competing interests to declare.

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Name: Gage Kromer

News Article: Problematic Alcohol Consumption Linked To Genetics - BioTechniques

Short Description: Scientists uncover 29 new genes that are linked to problematic Alcoholism in humans.

Scientific paper: https://www.nature.com/articles/s41593-020-0643-5

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Understanding the genetics of alcoholism: 29 gene variants identified

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Nineteen novel genetic variants associated with problematic alcohol consumption have been identified in a genome-wide analysis.