In general, the efficacy of PARP inhibitors for treatment of cancers with BER and alt-EJ repair defects is due to such lethal synergistic interactions.428,429 In 2005, Helen EB et al. first indicated that knockout cells of BRCA2 showed defects in HE [Please define this abbreviation] pathway repair, which made the cells sensitive to PARP inhibitors and showed that PARP-1 activity is vital in HE-deficient BRCA2 mutant cells.430 Thus, in BRCA2 mutant cells, the replication fork lesion cannot be repaired and the cancer cells die. This evidence concerns the gene PARP1 and cancer.