Research, not limited to ovarian cancer, has demonstrated these complex mechanisms, including but not limited to: upregulation of the drug efflux transporter ABCB1, which enhances drug efflux; [33] mutations in PARP1 that reduce the affinity for PARPi; [34] loss of poly(ADP-ribose) glycohydrolase (PARG) that restores poly(ADP-ribosyl)ation (PARylation) and mitigates synthetic lethality; [35] reversal or reactivation of BRCA1/2 genes; [36–40] BRCA-independent homologous recombination restoration; [41] and recovery of replication fork stability [42, 43]. This evidence concerns the gene BRCA1 and ovarian cancer.