Proposed oncogenic mechanisms of hotspot p53 mutations include prolonged tumor necrosis factor alpha (TNF-α) signaling through the activation of NFĸB (nuclear factor kappa-light-chain-enhancer of activated B cells)11,12, causing chronic tumor-associated inflammation, as well as altered structural interaction between mutated p53 and DNA that induces transcriptional perturbations to promote tumor-associated gene expression13–15. Here, TP53 is linked to neoplasm.