Typically, TP53‐mutated cells accumulate excessive levels of mutant protein that is unable to transcriptionally transactivate canonical p53 target genes and may possess new, gain‐of‐function activities.3 A comprehensive study of the transactivational capability of p53 mutants, representing all possible amino acid substitutions caused by point mutation, demonstrated that human tumour‐associated mutations are strongly correlated with inactivation of p53 function.4 This evidence concerns the gene TP53 and neoplasm.