The discovery that small-molecule inhibitors of PARP as single agents could selectively kill BRCA1 and BRCA2 deficient cancer cells1,2 led to new therapeutic approaches for patients with gBRCAm and other associated DNA damage response (DDR) gene aberrations, including deficiencies in the homologous recombination repair (HRR) pathway3,4. This evidence concerns the gene BRCA1 and cancer.