ARHGAP6 is a Rho GTPase-activating protein that inactivates Rho-type GTPases by promoting GTP hydrolysis to the GDP-bound state 1. This catalytic activity regulates actin cytoskeleton dynamics and cell motility by promoting cytoplasmic process elongation while facilitating cell body retraction 2. ARHGAP6 also directly binds and activates phospholipase C-delta1, modulating its catalytic properties and calcium responsiveness 2. Clinically, ARHGAP6 exhibits context-dependent roles in cancer. In solid tumors, ARHGAP6 acts as a tumor suppressor: reduced ARHGAP6 expression correlates with poor prognosis in bladder cancer and breast cancer 34. ARHGAP6 suppresses bladder cancer cell viability, migration, and invasion via β-catenin signaling inhibition and enhances chemosensitivity to mitomycin C 3. In breast cancer, ARHGAP6 is transcriptionally repressed by ZBTB6, and its restoration attenuates STAT3 signaling to inhibit progression 4. ARHGAP6 also promotes ferroptosis in breast cancer through RhoA/ROCK1/p38 MAPK signaling 5. Conversely, in acute myeloid leukemia, high ARHGAP6 expression associates with poor overall and disease-free survival, suggesting an oncogenic function 6. Additionally, ARHGAP6 is involved in gastric cancer as part of fusion events (CLDN18-ARHGAP6) linked to specific molecular subtypes 7. ARHGAP6 depletion inhibits cervical carcinoma cell proliferation and promotes apoptosis via Rac3 targeting 8.