ATG9A is a ubiquitously expressed transmembrane phospholipid scramblase essential for autophagosome biogenesis 1. Its primary function involves mediating autophagosomal membrane expansion by cycling between the phagophore assembly site and cytoplasmic vesicles, supplying phospholipids for autophagosome growth 1. ATG9A's lipid scramblase activity distributes phospholipids across the bilayer to drive membrane expansion, while also recruiting phosphatidylinositol 4-kinase beta via ARFIP2 to supply phosphatidylinositol 4-phosphate for autophagosome initiation 1. Beyond autophagy, ATG9A has emerged with multiple non-canonical functions: it protects plasma membrane integrity through ESCRT cooperation 2, delivers PI4K2A to damaged lysosomes for repair via ARFIP2 interaction 3, and independently mediates galectin-9 secretion through specialized vesicle carriers 4. ATG9A deficiency causes severe cellular and organismal defects, including impaired oligodendrocyte differentiation and mitochondrial dynamics 5. In diabetes pathogenesis, dysregulated ATG9A expression contributes to pathological autophagy overload in pancreatic β-cells under glucolipotoxic stress 6. ATG9A's multi-functional roles position it as a critical regulator of cellular homeostasis beyond classical autophagy.