SLC38A2 is a sodium-dependent neutral amino acid transporter that mediates the cotransport of amino acids and sodium ions across the cell membrane with a 1:1 stoichiometry. The transporter functions at the blood-brain barrier and placenta, and maintains glutamine/glutamate balance critical for neuronal signaling. In cancer biology, SLC38A2 plays a central metabolic role by facilitating glutamine uptake, which fuels tumor growth and metastasis. In bladder cancer, ubiquitin-conjugating enzyme UBE2C stabilizes SLC38A2 at the cell membrane to enhance glutamine uptake, promoting lymphangiogenesis and lymph node metastasis 1. Similarly, in lung adenocarcinoma, cancer-associated fibroblasts upregulate SLC38A2 through the LINC01614/NF-κB axis to enhance cancer cell glutamine consumption 2. In breast cancer brain metastases, tumor-derived miR-199b-5p downregulates neuronal SLC38A2 to hijack neuron-astrocyte metabolic coupling and promote brain colonization 3. In ARID1A-mutant ovarian clear-cell carcinoma, SLC38A2 inhibition impairs alanine uptake and synergizes with immunotherapy 4. Clinically, SLC38A2 represents a therapeutic target. Genetic variants (rs1873793) associate with hypertension risk, and pharmacological inhibition with methylaminoisobutyric acid (MeAIB) lowers blood pressure in rodent hypertension models by suppressing endothelial glutamine uptake and activating the AKT-eNOS nitric oxide pathway 5. Pan-cancer analysis identifies SLC38A2 as a prognostic risk factor in breast cancer, lung adenocarcinoma, mesothelioma, and pancreatic adenocarcinoma, suggesting broad therapeutic potential 6.