Additionally, OC cells can develop PARPi resistance through various mechanisms, including the restoration of HR repair activity; replication stress mitigation, whereby the cancer cell slows the cell cycle and stabilizes replication forks; and mechanisms not currently assigned to a single DNA repair pathway-related process but still alter the response to PARPi, such as mutations in PARP itself, genomic events that change protein poly-ADP-ribosylation (PARylation), PARP trapping, upregulation of drug efflux pumps and activation of alternate pathways (Figure 3) [280]. This evidence concerns the gene PARP1 and cancer.