ARHGAP1 (Rho GTPase-activating protein 1) is a GAP protein that inactivates Rho family GTPases by converting them from active GTP-bound to inactive GDP-bound states, with Cdc42 as the preferred substrate 1. The protein localizes to multiple cellular compartments including the cytoplasm, plasma membrane, and endosomal structures, and participates in cadherin binding and signal transduction regulation 2. Mechanistically, ARHGAP1 modulates actin filament dynamics and endocytic transport. In influenza-infected cells, ARHGAP1 is transported with viral ribonucleoproteins via Rab11a-mediated endocytic pathways, where it stabilizes actin filaments to promote budozone formation 2. In neuronal contexts, Cdc42GAP deficiency impairs cognitive function and dendritic spine density through elevated Cdc42 signaling, suggesting ARHGAP1 regulates synaptic plasticity 1. Disease relevance includes Alzheimer's disease, where Cdc42GAP deficiency promotes tau hyperphosphorylation and amyloid accumulation through GSK-3β activation 1. In diabetic retinopathy, ARHGAP1 influences disease progression via body mass index, C-reactive protein, and hypertension regulation 3. Conversely, ARHGAP1 overexpression suppresses cervical carcinoma cell proliferation, migration, and invasion 4, while circRNA-mediated ARHGAP1 upregulation promotes breast cancer progression 5. In ischemic cardiomyopathy, ARHGAP1 overexpression induces myocardial apoptosis through Bcl-2 pathway modulation 6.