ARHGAP19 is a Rho GTPase-activating protein that negatively regulates RhoA signaling by catalyzing GTP hydrolysis to convert Rho GTPases to their inactive GDP-bound state 1. The protein localizes to multiple cellular compartments including the cytoplasm, plasma membrane, nucleus, and equatorial cell cortex, with subcellular positioning dynamically regulated by CDK1 and ROCK-mediated phosphorylation during mitosis 2. ARHGAP19 is essential for cell division, controlling cytokinesis, chromosome 10, and proper recruitment of contractile machinery components including citron and myosin II to the mitotic cleavage furrow in T lymphocytes 1. Loss-of-function mutations in ARHGAP19 cause autosomal recessive Charcot-Marie-Tooth disease, a motor-predominant inherited neuropathy affecting 25 individuals from 20 families 3. Patient variants impair GAP activity and reduce protein levels, leading to axonal and synaptic morphology defects through dysregulation of motor proteins and cell cycle pathways 3. Beyond neurological function, ARHGAP19 participates in endometrial epithelial transformation during uterine receptivity establishment, where it remodels junctional complexes and cytoskeletal architecture to promote embryo implantation 4. Genetic variants associated with ARHGAP19 expression show suggestive association with supernormal coronary artery phenotypes 5. However, ARHGAP19 demonstrates no causal relationship with autism spectrum disorder 6.