This is particularly interesting given the advances in cancer treatment in tumor models that are defective in this pathway (taking advantage of synthetic lethality [93]), specifically with poly (ADP-ribose) polymerase (PARP) inhibitors; an in vitro study demonstrated the antitumor effect of this agent in monotherapy (dependent on the degree of HR deficiency and PARP1 expression) and, additionally, potentiated its sensitivity to cisplatin [92]. The gene discussed is PARP1; the disease is cancer.