RAB5B is a small GTPase that functions as a key regulator of early endocytic trafficking. It localizes to the plasma membrane and early endosomes 1, where it cycles between inactive GDP-bound and active GTP-bound states to recruit effector proteins responsible for vesicle formation, movement, and fusion 23. RAB5B is specifically required for EEA1 recruitment to early endosomes and mediates endocytosis of growth factors like EGF and transferrin 23. Dysregulation of RAB5B is associated with multiple disease pathologies. In cancer, RAB5B expression correlates with tumor progression across diverse malignancies and modulates cell migration and adhesion 4. In pancreatic cancer, RAB5B participates in perineural invasion through extracellular vesicle-mediated circRNA delivery 5, while in breast cancer, RAB5B downregulation by miR-130a-3p inhibits cancer stem cell migration and invasion 6. Elevated RAB5B expression also correlates with insulin resistance in polycystic ovary syndrome, affecting PI3K/AKT and MAPK/ERK signaling pathways 7. Additionally, RAB5B upregulation promotes melanocore clustering in keratinocytes, relevant to melasma pathophysiology 8. These findings suggest RAB5B as a therapeutic target in multiple disease contexts.