SLC38A1 is a sodium-dependent symporter that mediates transport of short-chain neutral amino acids across the cell membrane, driven by the Na+ electrochemical gradient 1. The transporter exhibits 1:1 Na+:amino acid stoichiometry and is expressed prominently in placenta and heart, with detectable levels in brain and other tissues 1. SLC38A1 participates in glutamine transport into retinal tissue and may contribute to placental trophoblast amino acid handling and synaptic plasticity regulation. In cancer biology, SLC38A1 expression is significantly elevated in multiple tumor types including colorectal cancer, hepatocellular carcinoma, and oral squamous cell carcinoma compared to adjacent normal tissues. In colorectal cancer, high SLC38A1 expression correlates with tumor node metastasis stage and promotes cell proliferation and migration 2. In hepatocellular carcinoma, OTUD5-mediated deubiquitination stabilizes SLC38A1 protein, enhancing HCC cell proliferation 3. Additionally, in breast cancer patients, elevated SLC38A1 expression associates with poor prognosis 4. Recent evidence indicates SLC38A1 functions as an amino acid metabolism node in diverse pathological contexts. In selective intrauterine growth restriction, miR-373-3p suppresses SLC38A1 expression via HIF-1α-dependent mechanisms, impairing trophoblast cell migration 5. In retinal pigment epithelium, complement C5a promotes cell viability and migration through SLC38A1-mediated glutamine metabolism 6. SLC38A1 upregulation represents a potential therapeutic target across multiple cancer types and metabolic disorders.