SLC38A4 encodes SNAT4, a sodium-dependent symporter that mediates electrogenic, pH-dependent cotransport of neutral amino acids (particularly glycine, alanine, serine, asparagine, and threonine) across the plasma membrane 123. The transporter preferentially recognizes smaller amino acids and tolerates partial lithium substitution for sodium 4. Clinically, SLC38A4 polymorphisms associate with glucose metabolism: the 1304 G>A SNP correlates with hyperglycemia in adults 5, while the 292 C>T SNP associates with elevated neonatal glucose 6. In placental physiology, SLC38A4 expression correlates with fetal growth—increased expression in macrosomic pregnancies and decreased expression in early preterm intrauterine growth restriction 78. SLC38A4 expression is sensitive to glucose deprivation and hypoxia in trophoblasts, suggesting nutrient-sensing functions 8. Beyond amino acid transport, SLC38A4 functions as a tumor suppressor in hepatocellular carcinoma, where its downregulation promotes proliferation via Wnt/β-catenin/MYC pathway activation 9. In pancreatic α-cells, SLC38A4 upregulation following glucagon receptor inhibition drives α-cell proliferation through mTORC1 activation 1011. These findings reveal SLC38A4's broader roles in glucose homeostasis, fetal development, and metabolic disease pathogenesis.