These therapies are rooted in the concept of synthetic lethality wherein deficiency in BRCA1 and/or BRCA2 or other homologous recombination (HR)-associated genes in the tumor renders tumor cells sensitive to PARP inhibition by disabling a PARP-dependent single-stranded DNA (ssDNA) repair pathway in the context of defective HR DNA repair, which is dependent on BRCA1,BRCA2 and associated factors4. Here, BRCA1 is linked to neoplasm.