Therefore, targeting CHK2 (BML-277, also binding to the ATP pocket) blunted PARP inhibitor toxicity in p53-wild-type pro-B/pre-B cells but not in p53-deficient ovarian cancer cells, indicating that CHK2 inhibition may be a promising chemoprotective mechanism that can be leveraged to maintain olaparib efficacy [173]. The gene discussed is CHEK2; the disease is ovarian cancer.