ARHGAP29 is a Rho GTPase-activating protein that inactivates RhoA, RAC1, and CDC42 by promoting GTP hydrolysis to the GDP-bound state 1. Primary function involves converting active Rho GTPases to inactive forms, with preferential activity toward RhoA 2. Mechanistically, ARHGAP29 operates within multiple signaling contexts: it functions as a RAP2A effector in ECM mechanotransduction, where low matrix stiffness activates RAP2, which stimulates ARHGAP29 to suppress YAP/TAZ through LATS1/2 activation 3. In podocytes, ARHGAP29 expression is YAP/TAZ-dependent and regulates RhoA signaling critical for lamellipodia formation and integrin adhesion dynamics 1. ARHGAP29 transcription is regulated by SMARCA4 (SWI/SNF complex) and TBX21, establishing it as a tumor suppressor in triple-negative breast cancer and colorectal cancer by suppressing RhoA hyperactivation 2, 4. In keratinocytes, ARHGAP29 regulates cell morphology, proliferation, and migration through RhoA/ROCK signaling, though it is dispensable for in vivo wound healing 5. Disease relevance includes nonsyndromic cleft lip/palate, where ARHGAP29 variants impair craniofacial development through IRF6 pathway interactions 6, and glioblastoma progression through morphological phenotype switching 7.