Although typically regarded as pro-survival under physiological conditions, studies in which PARP1 was inhibited during S-phase in BRCA1- and BRCA2-deficient cells have shown that PARP1 inhibition causes genomic instability, cell-cycle arrest, and apoptosis, as these cells were defective in homology-directed double-strand break repair mechanisms [17–19] imparted by unmutated BRCA1. Importantly, hereditary breast cancers due to mutations in BRCA1 are mainly of the basal-like or TN subtypes suggesting the utility of PARP1 inhibitors in treatment of patients with TN breast cancer. This evidence concerns the gene BRCA1 and breast carcinoma.