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The authors showed that IKK triggered p53 phosphorylation and acetylation, upregulating the expression of its pro-apoptotic target genes [44]

p53 phosphorylation and association with murine double minute 2, c-Jun NH2-terminal kinase, p14 ARF , and p300/CBP during the cell cycle and after exposure to ultraviolet irradiation

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Upon UVR-induced DNA damage, different pathways lead to the dissociation of the p53/mouse double minute 2 (MDM2) inhibitory complex [28] and two major kinases, ataxia telangiectasia mutated (ATM) and ataxia telangiectasia and Rad3-related (ATR), mediate p53 phosphorylation, preventing its degradation [29]

This type of mutation is infrequent in most other tumors aside from hepatocellular carcinoma