It has been shown that different tumors with an inability to fix DNA double-strand breaks (DSB) by homologous recombination repair (HRR), such as those with alterations in the breast cancer 1 and 2 (BRCA1 and BRCA2) genes, are very responsive to an emerging therapeutic approach, represented by the inhibition of the poly (ADP-ribose) polymerase (PARP) enzyme. Here, PARP1 is linked to breast carcinoma.