The investigators found that as CD8+ T cells activated by anti-PD-L1 immunotherapy secreted interferon-gamma (IFN-γ) after PD-L1 blockade, IFN-γ significantly downregulates SLC7A11 and SLC3A2 expression in tumor cells through activation of JAK1-STAT1 signaling, leading to reduced cystine uptake, enhanced lipid peroxidation and subsequent ferroptosis (Figure 2). The gene discussed is CD8A; the disease is neoplasm.