It is well established that the dependency on alternative DNA repair mechanisms due to defective homologous recombination renders cancer cells with defects in genes associated with the BRCAness phenotype or replication stress susceptible to the targeted inhibition of poly‐(adenosine 5′‐diphosphate ribose) polymerase (PARP) or the ataxia telangiectasia and Rad 3 related‐CHK1‐WEE1 axis.47 This evidence concerns the gene CHEK1 and cancer.