In contrast, in cancer cells with wild-type TP53; ataxia telangiectasia-mutated (ATM); and its targets, p53 and checkpoint kinase 2 (CHK2), were more strongly activated by the addition of DNA-PKcs inhibitor M3814, leading to a complete p53-dependent cell-cycle block and premature cell senescence [70]. This evidence concerns the gene PRKDC and cancer.