RALB (RAS like proto-oncogene B) is a multifunctional GTPase that regulates diverse cellular processes including gene expression, cell migration, proliferation, and membrane trafficking 123. As a GTP-dependent molecular switch, RALB functions by interacting with distinct downstream effectors to control exocytosis of dense-core vesicles, exocyst complex assembly and localization, and suppression of apoptosis 42. RALB mediates abscission during late cytokinesis and regulates ligand-dependent endocytosis of growth factor receptors 31. Calmodulin binds RALB in a calcium-dependent manner, regulating its activation 5. In cancer biology, RALB emerges as a critical oncogenic mediator across multiple malignancies. RALB signaling is hyperactivated in acute myeloid leukemia (AML) patient samples and promotes leukemic cell survival 6. RALB promotes lymph node metastasis in tongue squamous cell carcinoma and serves as a prognostic factor in head and neck cancers 7. In colorectal cancer, the butyrate/OR51E1/RALB axis facilitates radiation-induced autophagy, sensitizing tumors to radiotherapy 8. RALB degradation by dihydroartemisinin triggers autophagy and suppresses the IFI16/caspase-1 inflammasome in laryngeal cancer 9. Additionally, elevated RALB in circulating extracellular vesicles correlates with poor clinical prognosis in pancreatic cancer 10. These findings position RALB as a promising therapeutic target across diverse cancer types.