SLC38A5 (SNAT5) is a sodium-dependent neutral amino acid symporter that mediates bidirectional transport of glutamine, asparagine, serine, glycine, and alanine coupled with Na+ influx and H+ efflux 1. The transporter functions in metabolically active tissues including brain, liver, pancreas, and retina, where it participates in glutamine-glutamate cycling 2. SLC38A5 expression is regulated by mTORC1 and Wnt/β-catenin signaling pathways and is sensitive to pH, nutritional stress, and inflammation 1. Clinically, SLC38A5 is markedly upregulated across multiple cancers, promoting tumor progression through glutamine-dependent metabolic reprogramming. In pancreatic cancer, SLC38A5 overexpression confers gemcitabine resistance by suppressing ferroptosis via mTOR-SREBP1-SCD1 signaling 3. Similarly, in osteosarcoma and breast cancer, SLC38A5 enhances proliferation and chemoresistance through PI3K/AKT/mTOR activation 45. In colorectal cancer, SLC38A5 drives ferroptosis resistance via Hippo-YAP/Nrf2 signaling 6. SLC38A5 is essential for asparagine-dependent acute lymphoblastic leukemia cell survival 7. Additionally, SLC38A5 regulates developmental retinal angiogenesis through Wnt signaling and promotes inflammatory dendritic cell responses in psoriasis via lysosomal acidification 28. These findings establish SLC38A5 as a promising therapeutic target for cancer and inflammatory diseases.