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Differential binding analysis of the activating histone mark H3K4me3 (associated with transcription start sites) revealed significant enrichment in MEC-1/N M cells at genes associated with mitochondrial transcription and translation, in both untreated (UN) and BCR-stimulated (IgM) conditions (TableS6-7)

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So far, studies have not shown any genotoxic or carcinogenic effects associated with these peptides

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Studies have confirmed (121, 122) that p53 can induce ferroptosis not only by inhibiting SLC7A11 activity but also by increasing CDKN1A expression or decreasing DPP4 activity, suggesting the dual regulatory role of p53 in the regulation of ferroptosis