Another benefit of using PARP inhibitors as DNA repair modulators acting at the level of the epigenome comes from the observation that poly-ADP-ribosylation is a co-activator of cell cycle-dependent genes that are simultaneously controlled by BRG1 and EP300, and are mostly over-expressed in the studied breast cancer cells, thus providing some selectivity toward this group. This evidence concerns the gene PARP1 and breast cancer.