Consistently, emerging studies indicated that modulation of oxidative stress, ablation of CD36 (a scavenger receptor known for its function as a fatty acid transporter) (43, 44), or overexpression of GPX4 (44, 45) suppressed lipid peroxidation, restored tumor-infiltrating CD8+ effector functions, and enabled tumor control. The gene discussed is CD8A; the disease is neoplasm.