RASAL2 (RAS protein activator like 2) is a RasGAP that inhibits the Ras-cyclic AMP signaling pathway through GTPase activator activity 1. However, RASAL2 exhibits context-dependent and paradoxical roles in cancer biology. In breast cancer, RASAL2 functions as a tumor and metastasis suppressor, with loss associated with metastatic disease and chemoresistance 1. Yet in other malignancies, RASAL2 acts as an oncogene. In gastric cancer, H. pylori infection induces RASAL2 expression via NF-κB, which then activates the AKT/β-catenin axis by inhibiting protein phosphatase 2A, promoting tumorigenesis 2. Similarly, RASAL2 is upregulated in hepatocellular carcinoma and pancreatic ductal adenocarcinoma, where it promotes proliferation and metastasis 3 4. RASQL2 regulates multiple pathways beyond Ras signaling. In astrocytomas, it modulates RHO activity and mesenchymal-amoeboid transition 5. In triple-negative breast cancer, RASAL2 knockout increases autophagic-exosome secretion via Rab27a regulation 6, and RASAL2 confers chemoresistance through CREB1-BCL2-mediated mitochondrial apoptosis resistance 7. In chr1 kidney disease, RASAL2 suppresses angiogenesis and promotes peritubular capillary rarefaction via HIF-1α 8. These findings establish RASAL2 as a multifunctional signaling hub with tissue- and context-specific roles in cancer progression and fibrotic disease.