SLC38A2 is a sodium-dependent neutral amino acid symporter that mediates cotransport of amino acids and sodium ions across the plasma membrane with 1:1 stoichiometry 12. The transporter functions at critical physiological barriers, including the blood-brain barrier and placenta 12, and plays specialized roles in glutamine homeostasis and bone development through proline transport. Mechanistically, SLC38A2 exhibits pH-sensitive, electrogenic transport driven by the sodium electrochemical gradient and is intolerant to lithium 1. Protein stability is regulated through ubiquitination-mediated membrane localization, with monoubiquitination at lysine 59 suppressing endocytosis 3. The transporter's expression is tightly controlled by transcriptional regulators and inflammatory signaling pathways 45. Clinically, SLC38A2 dysregulation is implicated in multiple pathologies. In hypertension, SLC38A2 inhibition lowers blood pressure by modulating endothelial nitric oxide signaling through glutamine uptake regulation; the rs1873793 variant associates with hypertension risk 6. In cancer, SLC38A2 upregulation promotes glutamine addiction in lung adenocarcinoma and bladder cancer metastasis 43, while brain metastasis involves miR-199b-5p-mediated SLC38A2 downregulation in neurons to reprogram neural metabolism 7. ARID1A-mutant ovarian cancers exhibit SLC38A2 dependence exploitable therapeutically 8. In allergic rhinitis, SLC38A2 mediates alanine uptake by dendritic cells through CD169+ macrophage signaling 9.