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Activation of p53 could not directly induce ferroptosis, but it can inhibit the expression of SLC7A11 by promoting nuclear translocation of the deubiquitinase USP7 and then decreasing the occupancy of monoubiquitination of histone H2B on lysine 120 (H2Bub1) in the regulatory region of SLC7A11 gene [100]

10.1038/s41598-017-11065-8 Sci

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These observations point to a global reprogramming of circadian gene expression, rather than a disruption that may confer a physiological advantage to tumor cells and prompt to suggest that clock dysfunction could be considered a pro-tumoral event, thus indicating clock dysfunction as a potential hallmark of cancer