Some DNA repair deficiencies are known to modulate the response to therapies: BRCA1/2 deficiency renders cancers susceptible to treatment with PARP inhibitors (Bryant et al., 2007), mismatch repair (MMR)-deficient cancers are sensitive to checkpoint inhibitors (Le et al., 2015) but resistant to alkylating agents such as temozolamide (von Bueren et al., 2012), and CDK12-mutated cancers have a suggested sensitivity to CHK1 inhibitors (Paculová et al., 2017). This evidence concerns the gene CHEK1 and cancer.