IFNγ produced by CD8+ T cells increases the activity of lipid peroxidation in tumor cells.[25] In addition, IFNγ upregulates ACSL4 expression via STAT1 and IRF1 signaling and reprograms tumor fatty acid metabolism.[26] Through these two nonoverlapping mechanisms, tumor‐reactive CD8+ T cells control tumor growth by inducing ferroptosis. The gene discussed is ACSL4; the disease is neoplasm.