In addition, immunotherapy-activated CD8+ T cells promote tumor ferroptosis by releasing IFN-γ, which suppresses SLC3A2 and SLC7A11 expression, reduces cystine uptake, and increases lipid peroxidation—thereby enhancing antitumor efficacy and suggesting ferroptosis as a synergistic mechanism with checkpoint blockade therapy (70). The gene discussed is SLC3A2; the disease is neoplasm.