A systematic genetic analysis comprising seven genome-wide screens in haploid human cells uncovered new regulatory mechanisms at most levels in the WNT signaling pathway.

Transient transcriptome sequencing and kinetic modeling suggest how the kinetics and yield of RNA splicing are encoded in the human genome.

A gene-centric functional screen uncovers biological mechanisms underlying genome-wide association study signals for human red blood cell traits.

An integrative approach, combining genetic mouse and large-scale human genetics studies, was used to reveal a novel role for the Bcl-2 protein Bid in maintenance of mitochondrial function that alters susceptibility to myocardial infarction.

Although cellular organelles show a functional deterioration in aging, genetic loci associated with common age-associated disease instead nominate nuclear transcription factors across several age-related diseases.

Common nuclear genetic variants are associated with fundamental biological processes occurring in human mitochondria and potentially point to novel roles for nuclear genes in transcriptional regulation of the mitochondrial genome.

It is always better to use mixed effects models over principal components association regression for genetic association studies of continuous traits, since the former models family structure and close relatives are always found in real human studies.

A CRISPR-based method enables targeted knockouts and genetic screens in human dendritic cells.

An innovative strategy in genome analysis has generated a detailed description of how pathogens mutate when facing human genetic diversity.

There is limited epigenetic conservation of lineage-specific DNA elements in Treg cells, and genetic variation in Treg cell specific enhancers is associated with autoimmune disease.