A viable separation of function XRCC4 knock-in mutant mouse model recapitulates some aspects of XRCC4 deficiency in humans, notably the absence of immune deficiency.

Anchoring of proteins to the cell membrane through the glycosylphosphatidylinositol (GPI) anchor is critical for the survival of the cells that will give rise to the brain and face.

Loss of myelin integrity in the mouse forebrain perturbs executive functions, assessed by tests requiring normal motor performance.

Altering the level of different oncogenic mutants of Kras induces unique tumor patterns in mice, suggesting that tissue-specific responses mold the sensitivity of normal tissues to different oncogenic RAS mutations.

The developmental transcription factor TBX3 co-operates with β-catenin co-factors to operate tissue-specific transcriptional outputs, during forelimb development and colorectal cancer progression.

Acute one-hour treatment of Pik3ca mutant mice with a novel anti-epilepsy drug suppresses seizures despite continued developmental brain dysmorphology, promising a new therapeutic strategy for patients with intractable pediatric epilepsy.

Dystonin-b-specific mutant mice exhibit late-onset myopathy and cardiomyopathy.

A new knock-in mouse endogenously labels cytotoxic granules and can be used with all modern super-resolution imaging techniques to study T cell function in vitro and in vivo.

RNF213 is a giant E3 ligase with a dynein-like core and a unique ubiquitination mechanism that proceeds in a RING-independent manner and is linked with the Moyamoya disease.

BAP1/ASXL is a key regulator of trophoblast invasion during early mouse and human placentation.