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As a consequence, the unrestrained and potentially lethal accumulation of ROS threatens to damage many biomolecules: lipids, proteins, DNA, and host cells

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Notably, the acetylation-defective mutant p53 3 KR, which cannot induce cell-cycle arrest, senescence or apoptosis, fully retains the ability to suppress SLC7A11 and trigger ferroptosis under oxidative stress (Le et al., 2015)