SLC7A6 (y+LAT2) is a transmembrane antiporter that functions as part of the system y+L amino acid transport system 1. As a heterodimer with SLC3A2 (4F2hc), SLC7A6 mediates electroneutral, 1:1 stoichiometry exchange of cationic amino acids (L-arginine, L-lysine) for neutral amino acids (L-leucine, L-glutamine) in a sodium-independent manner, while also transporting neutral amino acids in a sodium-dependent fashion 1. This transport activity supports the glutamate-glutamine cycle and ammonia clearance 1. SLC7A6 participates in nitric oxide synthesis through L-arginine availability 2. Clinically, SLC7A6 has emerged as a significant cancer-associated transporter. Elevated SLC7A6 expression correlates with poor prognosis across multiple cancers including hepatocellular carcinoma, cholangiocarcinoma, and pancreatic cancer 2. In hepatocellular carcinoma, SLC7A6 upregulation is part of global glutamine transporter reprogramming associated with worse survival 3. SLC7A6 promotes tumor progression by enhancing amino acid uptake and mTORC1 activation 1, regulating ferroptosis through redox homeostasis disruption 2, and supporting glutamine-driven cancer metabolism 4. High SLC7A6 expression negatively correlates with CD8+ T cell infiltration in cisplatin-resistant bladder cancer 5. These findings suggest SLC7A6 as a therapeutic target for cancer treatment.