Laboratory-based studies of BRCA1 and BRCA2 demonstrated that loss of function of either gene resulted in significantly increased susceptibility to certain forms of chemotherapy, including interstrand DNA cross-linking agents such as the platinum drugs and mitomycin C. More recently, loss of BRCA1 or BRCA2 function has also been shown to increase sensitivity to PARP inhibition, a finding made possible as a result of increased understanding of the DNA repair implications of BRCA1 or BRCA2 loss. To a large extent, these laboratory-based observations have now been verified in clinical trials enrolling patients with hereditary breast cancer. The implications of the discovery of BRCA1 and BRCA2 for treatment options in sporadic breast cancer are more complex. Based on a series of striking phenotypic similarities between the majority of sporadic triple-negative breast cancers and most cancers that arise in BRCA1 heterozygotes, the hypothesis arose that perhaps many of these sporadic cancers might also share a similar lesion in DNA repair (BRCAness) with the BRCA1-related tumors. This notion has now been put to the test in ongoing clinical trials that treat sporadic triple-negative breast cancer patients with platinum agents, PARP inhibitors, or combinations. The current evidence for and against this hypothesis will be discussed.