SERINC2 is a non-ATP-dependent lipid transporter that catalyzes bidirectional scrambling of phosphatidylserine, phosphatidylcholine, and phosphatidylethanolamine across cell membranes. Unlike SERINC3 and SERINC5, human SERINC2 does not restrict HIV-1 infectivity. Recent studies have revealed multiple disease-relevant functions beyond its canonical role. In cervical cancer, SERINC2 is highly expressed and promotes tumor progression through serine-dependent metabolic reprogramming; knockdown suppresses cell viability and induces apoptosis via the Myc pathway, which regulates glycolytic enzymes and epithelial-mesenchymal transition markers 12. SERINC2 also mediates immunosuppression by competing with CD8+ T cells for serine, driving T cell exhaustion in the tumor microenvironment 1. In bipolar disorder type II, SERINC2 expression is reduced in patient plasma, and microglial SERINC2 deficiency impairs phospholipid synthesis and synaptic pruning, contributing to depression-like phenotypes 3. In cardiac pathology, SERINC2 antagonizes mTORC1 signaling at the lysosomal membrane, protecting against pressure overload-induced hypertrophy 4. Genome-wide association studies identified SERINC2 as a risk locus for alcohol dependence in subjects of European descent 56. These findings establish SERINC2 as a pleiotropic regulator linking lipid metabolism to immune function, neural homeostasis, and cardiac remodeling.