Previous studies revealed that in response to genotoxic stress, p53‐deficient tumor cells may arrest in the S and G2 phases via Chk1 activation to allow time for DNA repair and that Chk1 inhibitors selectively potentiate the effects of DNA‐damaging agents, such as chemotherapy or radiation, in TP53‐mutated cancer cells (Zhao et al, 2002; Ma et al, 2011). Here, CHEK1 is linked to neoplasm.