TBC1D16 is a GTPase-activating protein (GAP) that primarily functions to regulate intracellular trafficking through modulation of Rab GTPases. TBC1D16 enhances the intrinsic GTP hydrolysis rate of Rab4A, thereby controlling receptor recycling from endocytic compartments to the plasma membrane 1. The protein localizes to both cytosol and early endosomes, where it colocalizes with transferrin and EGF receptors 1. Functionally, TBC1D16 reduces transferrin receptor recycling and enhances EGF-stimulated EGFR degradation, leading to decreased EGFR levels and signaling 1. TBC1D16 also acts as a GAP for Rab5C and can inhibit prototype foamy virus replication through promotion of IFN-β production 2. In cancer contexts, TBC1D16 shows complex roles: it is regulated by super enhancers in colorectal cancer 3, exhibits characteristic DNA methylation changes associated with tumor progression 4, and serves as a predictor of chemosensitivity in acute myeloid leukemia 5. Clinically, high TBC1D16 expression correlates with favorable prognosis in epithelial ovarian cancer 6, suggesting tissue-specific roles in cancer progression.