In cancer therapy, targeting a specific defect in tumor cells (e.g. HR deficiency due to BRCA mutations) and pharmacologically inhibiting its compensatory pathway [e.g. poly-ADP ribose polymerase (PARP)-mediated opportunistic repair] can induce a “lethal vulnerability” absent in normal cells, selectively killing cancer cell [4, 11]. The gene discussed is PARP1; the disease is neoplasm.