For example, approximately thirty point mutation signatures [12, 13] are known to exhibit variability in different cancers, with several either known to be connected to specific kinds of hypermutability defects (e.g., pol-ε defect [14], APOBEC defect [15], or various DNA mismatch repair defects such as those are induced by germline BRCA1 or BRCA2 mutations [16]), as well as distinct signatures of copy number or structural variation mechanisms [17, 18], such as those due to TP53 dysfunction [19, 20]. This evidence concerns the gene TP53 and cancer.