RAB11A is a small GTPase that functions as a master regulator of intracellular membrane trafficking by cycling between inactive GDP-bound and active GTP-bound forms to recruit effector proteins governing vesicle formation, movement, tethering, and fusion 1. Its primary role involves regulating endocytic recycling and forming a functional complex with RAB11FIP3 and dynein to move sorting endosomes along microtubules toward the centrosome 2. RAB11A coordinates membrane delivery during cytokinesis and participates in epithelial cell polarization through interactions with MYO5B and RAB8A 13. Additionally, RAB11A regulates ciliogenesis by promoting preciliary vesicular trafficking through a ciliary targeting complex, though phosphorylated WDR44 can inhibit this pathway upon LPAR1 signaling 4. Beyond trafficking, RAB11A modulates GAT-3 functional expression in astrocytes, influencing striatal neuromodulation and obsessive-compulsive-like behaviors 5. Clinically, RAB11A mutations cause developmental and epileptic encephalopathy, with de novo point mutations identified as a significant genetic etiology 6. In cancer contexts, RAB11A exhibits dual characteristics—promoting exosome secretion and tumor progression in breast cancer while regulating HER2 recycling relevant to anti-HER2 therapy resistance 78. RAB11A upregulation in acute respiratory distress syndrome monocytes suggests pathogenic involvement in inflammatory lung disease 9.