It has been postulated that selective inhibition of CHK2 could increase the efficacy of genotoxic cancer therapies in a p53 mutant background by modulating resistance pathways and may also be radioprotective to normal p53 wild-type tissues.1,2 Recent results demonstrate that selective inhibition of CHK2 in combination with PARP inhibition could also be therapeutically beneficial in cancer therapy.3 This evidence concerns the gene TP53 and cancer.