VPS13C encodes a bridge-like lipid transfer protein that mediates lipid transport between the endoplasmic reticulum (ER) and other organelles, particularly late endosomes/lysosomes 1. The protein contains a tubular N-terminal domain with a hydrophobic cavity capable of solubilizing and transporting glycerolipids between membranes 1. VPS13C localizes to ER contact sites where it tethers ER membranes to late endosomes/lysosomes and lipid droplets 1. The protein functions as a sensor of lysosome stress, rapidly relocating from cytosol to damaged lysosome surfaces in a Rab7-dependent manner to facilitate ER-lysosome contacts and lipid delivery 2. In dopaminergic neurons, VPS13C regulates lysosomal morphology, dynamics, motility, and hydrolytic activity through interactions with phospho-Rab10 3. Loss-of-function mutations in VPS13C cause autosomal recessive early-onset Parkinson's disease (PARK23) and dementia with Lewy bodies 45. VPS13C depletion leads to lysosomal dysfunction with altered lipid profiles, accumulation of mitochondrial DNA in the cytosol, and inappropriate activation of the cGAS-STING innate immune pathway 6. These findings implicate defects in ER-lysosome lipid homeostasis as a key mechanism in VPS13C-related neurodegeneration.