This combined strategy operates through multiple synergistic mechanisms: ferroptosis inducers (e.g., RSL3, sorafenib) directly promote tumor cell death (243, 244), while the release of DAMPs, such as HMGB1, from ferroptotic cells activates dendritic cells and recruits CD8+ T lymphocytes, transforming an immunosuppressive “cold” tumor microenvironment into an immunostimulatory “hot” one (151). This evidence concerns the gene CD8A and neoplasm.