TBC1D10B is a Rab GTPase-activating protein (RabGAP) that inactivates RAB3A, RAB22A, RAB27A, and RAB35 1. Its primary function involves regulating endocytic trafficking and endosomal dynamics. TBC1D10B is essential for tubular endosome formation, where it reduces active RAB22A levels and controls early endosome size in a GAP-activity-dependent manner 1. In vascular signaling, TBC1D10B suppresses VEGFR2-mediated angiogenic responses by lowering Erk1/2 and p38 phosphorylation while reducing VEGFR2 and NRP1 expression on filopodia 2. In neurodegeneration, TBC1D10B participates in tau clearance through a BAG3-HSP70-TBC1D10B-RAB35 regulatory axis that promotes endosomal sorting complex-mediated protein degradation 3. However, TBC1D10B shows significantly reduced colocalization with BAG3 in Alzheimer's disease brains, suggesting pathway dysregulation contributes to pathogenesis 3. Pathologically, TBC1D10B is upregulated in colon cancer and promotes tumor progression via PAK4-mediated activation of the PI3K/AKT/mTOR pathway, correlating with poor prognosis 4. Additionally, TBC1D10B dysregulation is implicated in hematologic malignancies, with TCR fusion-driven overexpression detected in pediatric B-cell lymphoblastic leukemia 5. These findings establish TBC1D10B as both a critical endosomal trafficking regulator and an emerging oncogenic driver.