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 Here, CHEK2 is linked to cancer.