ASAP3 (ArfGAP with SH3 domain, ankyrin repeat and PH domain 3) is an Arf-specific GTPase-activating protein that functions primarily as a regulator of cell migration and proliferation through Arf6 GTPase signaling 1. Mechanistically, ASAP3 localizes to focal adhesions and circular dorsal ruffles where it regulates actin dynamics and stress fiber assembly 1. The protein modulates Arf1, Arf5, and Arf6 as substrates, with its catalytic activity enhanced by phosphatidylinositol 4,5-bisphosphate 1. Beyond cancer, ASAP3 regulates microvilli structure in gastric parietal cells through Arf6-GTP-dependent F-actin assembly, and plays a role in osteoblast differentiation under mechanical tension via miR-149 targeting 23. Clinically, ASAP3 overexpression is associated with poor prognosis across multiple cancer types including glioma, colorectal cancer, lung adenocarcinoma, and non-small cell lung cancer 4567. In colorectal cancer, ASAP3 promotes oncogenesis through NF-κB pathway activation via NEMO interaction, while in lung adenocarcinoma, HIF-1α directly induces ASAP3 expression under hypoxic conditions 56. ASAP3 represents a potential therapeutic target for gastric acid-related diseases and cancer progression 2.