VPS13D is a lipid transport protein that mediates inter-organellar lipid transfer, primarily functioning at membrane contact sites between the ER, mitochondria, lipid droplets, and peroxisomes 1. The protein contains a lipid transfer domain that binds glycerophospholipids and fatty acids 2, and coordinates fatty acid trafficking from lipid droplets to mitochondria through ESCRT-dependent membrane remodeling in conjunction with TSG101 2. VPS13D is recruited to mitochondria via Miro, a conserved GTPase that serves as a universal mitochondrial adaptor 13, and promotes mitochondrial clearance through autophagy (mitophagy). Loss of VPS13D impairs mitochondrial clearance, causing mitochondrial dysfunction, ultrastructural defects, and triggering cGAS-STING-dependent inflammation and neuronal cell death 4. Disease relevance: Biallelic VPS13D mutations cause autosomal recessive cerebellar ataxia, spastic paraplegia, and neurodevelopmental disorders characterized by movement dysfunction and progressive neurodegeneration 56. A common VPS13D variant (rs6685273) associates with increased IL-6 production and elevated septic shock mortality 7, implicating VPS13D in immune regulation. These findings establish VPS13D as critical for mitochondrial homeostasis, lipid metabolism, and neurological health.