Through HR, breast-cancer-susceptibility proteins 1 and 2 (BRCA1 and BRCA2) are responsible for the repair of the double-stranded DNA breaks caused by the PARP1-inhibition-induced accumulation of DNA lesions [10], and the inhibition of PARP1 sensitizes BRCA1/2-deficient cancer cells to cell-cycle arrest and apoptosis [11,12]. This evidence concerns the gene BRCA1 and cancer.