SLC1A5 is a neutral amino acid transporter with dual localization and critical roles in metabolism and immune regulation. At the plasma membrane, SLC1A5 functions as a glutamine transporter essential for nutrient uptake 1, while a mitochondrial SLC1A5 variant transports glutamine into mitochondria for metabolic reprogramming 2. In cancer biology, SLC1A5 is oncogenic across multiple malignancies. It participates in tumor-immune cell communication networks in liver cancer 3 and promotes glutamine-driven metabolic reprogramming that enhances ATP production, antioxidant synthesis, and chemotherapy resistance in pancreatic cancer 2. In acute myeloid leukemia, IGF2BP2 stabilizes SLC1A5 mRNA to support leukemia stem cell renewal through glutamine metabolism 4. SLC1A5 also mediates NRF2-driven growth in lung cancer via the NRF2/KLF5/SLC1A5 glutamine pathway, making it a therapeutic target 5. Beyond cancer, SLC1A5 upregulation drives polycystic ovary syndrome pathogenesis when androgen-induced, disrupting folliculogenesis through altered glutamine metabolism 6. Therapeutically, SLC1A5 inhibition enhances anti-tumor immunity by improving metabolic fitness of CAR-T and NK cells 7 and blocks bladder cancer lymphangiogenesis 8. These findings identify SLC1A5 as a multifaceted therapeutic target across oncologic and endocrine diseases.