While moderate ferroptosis may enhance tumor immunogenicity by promoting dendritic cell activation and CD8+ T-cell recruitment, excessive or chronic activation can drive immunosuppression through the accumulation of myeloid-derived suppressor cells (MDSCs), M2-like tumor-associated macrophages (TAMs), and regulatory T cells (Tregs), potentially favoring recurrence or metastasis [104,105,107]. This evidence concerns the gene CD8A and neoplasm.