Since an important study published in 2005 showed that tumor cells missing BRCA-1 or BRCA-2, critical tumor suppressor proteins involved in double-strand DNA break (DSB) repair via homologous recombination (HR), are more vulnerable to PARP family DNA repair enzyme inhibitors (Farmer et al., 2005), which has brought PARP inhibitors into the spotlight in the treatment of DNA repair-deficient tumors. This evidence concerns the gene PARP1 and neoplasm.