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Therapeutically, these cells can be further potentiated using agents that intensify iron release (e.g., NCOA4 activators), enhance ACSL4-mediated PUFA incorporation, or inhibit GPX4-stabilizing pathways ( Collectively, these strategies demonstrate that metabolically targeting TAM subsets is a powerful approach to controlling ferroptosis, suggesting multiple avenues for combination therapies that integrate ferroptosis inducers, immune checkpoint modulators, and metabolic inhibitors

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