ARHGAP30 is a Rho GTPase-activating protein (GAP) that primarily regulates RAC1 and RhoA signaling 1. Beyond its canonical GAP function, ARHGAP30 exhibits context-dependent roles in both immune and cancer biology. In T cell development, ARHGAP30 stabilizes active RAC1 through a non-canonical mechanism independent of its GAP activity, preventing proteasomal degradation and enabling proper thymocyte migration and thymic egress 2. Loss of ARHGAP30 causes severe T cell lymphopenia, establishing its critical role in peripheral T cell homeostasis. Conversely, ARHGAP30 is frequently overexpressed in ovarian cancer, where it promotes tumor progression through PI3K/AKT/mTOR pathway activation; ARHGAP30 knockdown suppresses cancer cell proliferation, migration, and invasiveness 34. In colorectal cancer, ARHGAP30 functions as a tumor suppressor by facilitating p53 acetylation at lysine 382 through P300 interaction, with reduced expression correlating with poor patient survival 5. In cervical cancer, ARHGAP30 overexpression suppresses growth through ribosome biogenesis inhibition via nucleolin ubiquitination, independent of GAP activity 6. In lung adenocarcinoma, DNA methylation-mediated suppression of ARHGAP30 impairs anti-tumor immunity 7. These findings reveal ARHGAP30 as a context-dependent regulator with divergent roles in different malignancies, suggesting its potential as a prognostic marker and therapeutic target.