RAB7B is a small GTPase that controls vesicular trafficking from late endosomes to the trans-Golgi network (TGN) 1. As a negative regulator of toll-like receptor signaling, RAB7B suppresses TLR4 and TLR9-triggered inflammatory responses in macrophages by promoting their lysosomal degradation 23. The protein cycles between GTP-bound active and GDP-bound inactive states, regulated by the GAP protein TBC1D5 1. Beyond canonical trafficking, RAB7B interacts with myosin II to coordinate cytoskeletal organization and influence cell migration through RhoA activation 4. RAB7B exhibits distinct functions from its homolog Rab7a, with splice isoforms showing specialized localizations and biological roles 5. In pathological contexts, RAB7B dysregulation contributes to obesity when overexpressed, as it suppresses autophagy-mediated lipid degradation through LRRK2 interaction 6. Notably, RAB7B shares significant cross-reactive epitopes with the KRAS G12V neoantigen, representing an important safety consideration for TCR-based cancer immunotherapies 7. RAB7B-mediated autophagy also regulates oral squamous cell carcinoma proliferation 8, suggesting therapeutic potential in cancer treatment.