SLC23A2 encodes SVCT2, a sodium-dependent L-ascorbate cotransporter that mediates electrogenic uptake of vitamin C with a stoichiometry of 2 Na+ for each ascorbate molecule. Unlike SVCT1, which is confined mainly to epithelial tissues, SVCT2 is distributed across metabolically active cells and specialized tissues including the brain, heart, placenta, and liver 1. The transporter maintains intracellular vitamin C levels, which are essential for enzymatic reactions and protection against oxidative damage. SLC23A2 regulates hematopoietic stem cell function through vitamin C-dependent mechanisms. Deletion of Slc23a2 from hematopoietic cells depletes intracellular ascorbate without altering plasma levels, increasing HSC quiescence and self-renewal potential upon transplantation 2. In a Mediterranean population, the rs1279386 (A>G) polymorphism in SLC23A2 was associated with lower plasma vitamin C concentrations and increased risk of primary open-angle glaucoma 3. Recent evidence suggests SLC23A2 functions in craniofacial development via the PI3K-AKT-mTOR pathway; knockdown reduced intracellular ascorbic acid and increased apoptosis in palatal mesenchymal cells, with associations to non-syndromic cleft palate 4. A 2025 study proposes that maternal exercise-induced upregulation of SLC23A2 expression, through TET2-mediated demethylation, contributes to transgenerational endurance benefits via enhanced mitochondrial biogenesis 5. Genetic variation in SLC23A2 may modulate disease risk through effects on systemic and cellular vitamin C homeostasis.