Elegant preclinical work by Bryant and colleagues [11] and Farmer and colleagues [12] demonstrating the increased sensitivity of BRCA1/2-deficient cells to PARP inhibition and the subsequent resistance to PARP inhibition on restoration of BRCA2 functionality provided the impetus for the use of PARP inhibitors in patients with BRCA1/2-associated cancers and subsequently in sporadic cancers that display ‘BRCAness’ (that is, have defective HR without germline BRCA1/2 mutations) [13]. Here, BRCA1 is linked to cancer.