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Rather than treating ferroptosis as a uniform vulnerability, clinical translation will probably succeed where patients can be stratified by (1) the architecture of antioxidant defenses (for example, FSP1/GPX4 balance), (2) the size and distribution of cellular CoQ pools, (3) lipid composition and peroxidation-prone membranes and (4) oncogenic programs that remodel redox metabolism (such as NRF2–KEAP1)