SLC7A11 (xCT) is a cystine/glutamate antiporter that forms a heterodimer with SLC3A2 and mediates 1:1 electroneutral exchange of extracellular L-cystine for intracellular L-glutamate across the plasma membrane 12. This sodium-independent transport is driven by high intracellular glutamate concentration and intracellular cystine reduction, providing cysteine for glutathione (GSH) biosynthesis and antioxidant defense 123. Beyond cystine transport, SLC7A11 inhibits ferroptosis—a regulated cell death driven by lipid peroxidation—through multiple mechanisms: it imports L-kynurenine for anti-ferroptotic signaling and functions as an atypical proton transporter facilitating slow lysosomal proton efflux 45. SLC7A11 expression is dysregulated in multiple cancers where overexpression promotes tumor growth by suppressing ferroptosis, though creating glucose and glutamine dependency 3. In hepatocellular carcinoma, ATF4-induced SLC7A11 prevents ferroptosis-driven hepatocyte death and inflammation, protecting against NASH-related carcinogenesis 6. Conversely, p53 represses SLC7A11 to sensitize cells to ferroptosis-mediated tumor suppression 7. In NASH, elevated SLC7A11 reduces ROS levels, activates AMPK signaling, and suppresses NLRP3 inflammasome-driven inflammation and fibrosis 8.