The study found that GPx4 deficiency did not inhibit the development of tumors, instead, the GPx4-related ferroptosis caused the cytotoxic CD8+T cell CXCL10 dependent immersion, which was offset by the PD-L1 upgradation of the tumor cell and the significant HMGB1-mediated MDSC infiltration, resulting in a tumor-inhibiting immune response. The gene discussed is HMGB1; the disease is neoplasm.