RABL3 is a small GTPase that functions as a critical regulator of RAS signaling and ciliogenesis. Mechanistically, RABL3 modulates KRAS prenylation through interaction with RAP1GDS1 (SmgGDS), a RAS GTPase chaperone 1, and cooperates with RAB11 to promote ciliary vesicle formation at the mother centriole during early ciliogenesis, with GTP-binding capacity being essential for this process 2. In cancer pathology, RABL3 overexpression promotes proliferation, migration, and invasion across multiple tumor types. In non-small cell lung cancer, high RABL3 expression correlates with poor survival through repression of MAPK8/9/10-mediated autophagy 3. In hepatocellular carcinoma, RABL3 is upregulated in 80.2% of tumors and associates with metastasis, advanced stage, and shortened survival 45. In oral squamous cell carcinoma, RABL3 knockdown suppresses proliferation and invasion via FAK/AKT pathway inactivation 6. Clinically, germline RABL3 mutations confer hereditary pancreatic cancer susceptibility and are implicated in RASopathy syndromes 1, establishing RABL3 as both a disease biomarker and potential therapeutic target for cancer treatment.