ARHGAP11A is a Rho GTPase-activating protein that inactivates Rho-family GTPases by promoting their conversion to an inactive GDP-bound state 1. Beyond this canonical catalytic function, ARHGAP11A exhibits context-dependent roles in human development and disease. During corticogenesis, ARHGAP11A maintains cortical progenitor identity and ventricular zone integrity through RHOA-ROCK signaling, with loss-of-function causing premature progenitor delamination and reduced neurogenic capacity 2. Subcellular mRNA localization and local translation of Arhgap11a in radial glial basal endfeet spatially regulate progenitor morphology and neuronal positioning 3. The hGID-GID4 E3 ligase complex targets ARHGAP11A for proteasomal degradation, with stabilization impairing cell migration through RhoA inactivation at the cell periphery 4. In cancer, ARHGAP11A functions as an oncogene rather than tumor suppressor. It is upregulated in pancreatic adenocarcinoma, basal-like breast cancer, hepatocellular carcinoma, and lung adenocarcinoma, where it promotes proliferation, cell cycle progression, EMT, and apoptosis resistance 5678. In hepatocellular carcinoma, ARHGAP11A exerts oncogenic effects via direct interaction with Rac1B independent of its GTPase-activating activity 7. These findings position ARHGAP11A as both a developmental regulator and cancer biomarker warranting therapeutic investigation.