Rucaparib induces cytotoxicity in tumor cells with homologous recombination deficiency through a mechanism known as synthetic lethality, wherein enzymatic inhibition of PARP proteins in the presence of defects in the homologous recombination repair pathway (e.g., mutations in BRCA1 or BRCA2) results in the accumulation of DNA damage and cell death [1, 4, 5]. This evidence concerns the gene PARP1 and neoplasm.