Mechanisms of SSB repair include base-excision repair, nucleotide excision repair, and mismatch excision repair, whereas DSB repair includes homologous recombination (HR) and non-homologous end-joining (NHEJ).327 The primary mechanism for inhibiting PARP in cancer therapy is synthetic lethality, which indicates two genomic alteration events that are each relatively innocuous individually but become lethal when they occur together.328 When PARP1/2 is pharmacologically inhibited, the accumulation of SSB by PARP inhibition can progress to DSB, which is usually repaired through HR. This evidence concerns the gene PARP1 and cancer.