Interestingly, CD8+ T cells exhibit bidirectional regulation in this process: the IFN-γ they secrete enhances tumor sensitivity to ferroptosis by downregulating the expression of SLC7A11 in tumor cells (44), but T cells themselves have increased GPX4 dependence due to their high metabolic demands and are prone to autologous ferroptosis during GPX4 inhibitor treatment. The gene discussed is GPX4; the disease is neoplasm.