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Finally, translational progress is bottlenecked by the lack of strategies to selectively manipulate p53s ferroptosis-regulating activity: activating its pro-ferroptotic function in cancer cells while preserving its anti-ferroptotic role in normal tissues remains a major challenge, and no validated biomarkers exist to predict which tumors will respond to p53-targeted ferroptosis therapies

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To ascertain which KGDD is driving the observed phenotype, we constructed a CRISPR knockout library of 64 KGDDs and performed a dropout screen in the presence of olaparib (Fig