The tumor immune microenvironment plays a central role in modulating ferroptosis susceptibility: CD8<sup>+</sup> T cell-derived IFNγ downregulates system Xc<sup>-</sup> and upregulates ACSL4, while other immune cells such as Tregs, MDSCs, and macrophages further fine-tune ferroptosis through cytokine and redox signaling. The gene discussed is ACSL4; the disease is neoplasm.