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In addition, GPX4 inhibitors remain challenging to use in vivo owing to their poor bioavailability, and pharmacological inhibition of GPX4 carries a substantial risk of systemic toxicity, as demonstrated in GPX4 knockout mouse models 25,26,27 Thus, modulating the CoQ 10 redox cycle, either by inhibiting ubiquinol (CoQ 10 H 2 , reduced) formation or altering oxidoreductase activity, has emerged as an alternative therapeutic strategy for ferroptosis-based cancer therapy