According to our findings, the activation of PARP1 transcription as a consequence of the transition of a cell from quiescence to proliferation may help the cancer cell gain the necessary adaptive physiology by acting at the genomic level in two ways: directly, by contributing to DNA repair machineries, and indirectly, by affecting the transcription of BRG1–EP300 targets, among others, which enable the cancer cell to rapidly divide and resist DNA damaging agents [12,20,21,22]. This evidence concerns the gene EP300 and cancer.