RAB5C is a small GTPase that belongs to the Rab family and serves as a key regulator of early endocytic trafficking and membrane vesicle dynamics. The protein cycles between inactive GDP-bound and active GTP-bound forms, with the active state recruiting downstream effectors responsible for vesicle formation, movement, and fusion 1. RAB5C is essential for EEA1 recruitment to early endosomes and facilitates endocytosis and trafficking of receptors including EGF and transferrin through early endosomes 1. Beyond endocytosis, RAB5C plays important roles in autophagy regulation by interacting with Beclin1 to upregulate LC3-II expression and promote autophagic processes 2. The protein also participates in lysosomal degradation pathways, directing proteins like ACC1 to lysosomes via P62-dependent selective autophagy 3. Disease relevance includes its involvement in hepatocellular carcinoma progression through ferroptosis suppression 3, angiogenesis regulation by preventing VEGFR2 degradation 4, and viral replication promotion 2. Clinically, de novo missense variants in RAB5C cause a neurodevelopmental disorder characterized by macrocephaly and developmental delay through dominant negative mechanisms that disrupt endocytic pathway function 1.