Herein, numerous preclinical researches investigated whether the antitumor activity of DNA-damaging agents in BRCA1-mutated breast cancers had a similar activity in BRCA1-methylated tumors, and the results demonstrated that the BRCA1 hypermethylation conferred the same extent of sensitivity to poly adeno-sine diphosphate-ribose polymerase-1 (PARP1) inhibitors and platinum-derived drugs as did the BRCA1 mutation53, 54, 55. The gene discussed is PARP1; the disease is breast cancer.