TBC1D20 is a GTPase-activating protein (GAP) with multi-functional roles in cellular homeostasis. Its primary function involves accelerating GTP hydrolysis of Rab small GTPases, particularly Rab1, Rab2, and Rab18, by over five orders of magnitude 1. TBC1D20 promotes RAB18 dissociation from endoplasmic reticulum membranes into the cytosol 2 and has recently been identified as a GAP for Rab11, coordinating vesicle transport and actin remodeling during ciliogenesis 3. Mechanistically, TBC1D20 regulates autophagosome maturation through its RAB1B GAP activity, maintaining autophagic flux essential for protein and organelle degradation 4. It also facilitates lipid droplet homeostasis by promoting DGAT2 redistribution from the ER to lipid droplet surfaces via Rab1b 5. Loss-of-function TBC1D20 mutations cause Warburg Micro Syndrome 4, a rare autosomal-recessive disorder characterized by congenital cataracts, intellectual disability, and abnormal sexual development 6. TBC1D20-deficient mice exhibit cataracts, male infertility, and disrupted acrosomal development 7. The syndrome also presents with neuronal autophagic dysfunction, leading to adult-onset motor deficits 4. Clinically, TBC1D20 dysfunction represents part of a broader class of autophagy-related neurodevelopmental disorders with overlapping multisystem manifestations 8, establishing TBC1D20 as critical for maintaining lens transparency, reproductive function, and neuronal homeostasis.