TBC1D10A encodes a GTPase-activating protein (GAP) that specifically targets RAB27A and RAB35, but not RAB2A, RAB3A, or RAB4A 1. The protein functions as a negative regulator of various membrane trafficking processes through its GAP activity toward RAB35. TBC1D10A inhibits exosome secretion in oligodendrocytes by inactivating RAB35, leading to intracellular accumulation of endosomal vesicles 2. In endothelial cells, TBC1D10A negatively regulates Weibel-Palade body exocytosis by targeting RAB35, which normally promotes secretion of hemostatic factors like von Willebrand factor 3. The protein also modulates autophagy by inhibiting RAB35-mediated recruitment of the autophagy receptor NDP52 to various targets including bacteria and damaged mitochondria 4. Additionally, TBC1D10A regulates cilium length and membrane composition by controlling RAB35 activity, affecting Sonic hedgehog signaling components and ciliary function 5. In angiogenesis, TBC1D10A influences VEGFR2 signaling pathways, with overexpression leading to increased ERK1/2 signaling 6. The gene has been implicated in severe COPD through whole exome sequencing studies, suggesting potential clinical relevance in respiratory disease 7.