Since cancer cells with defects in DSB repair pathways are particularly sensitive to poly (ADP-ribose) polymerase (PARP) inhibitors, the same study tested the potential synthetic lethality of SPOP inactivation with these drugs in vitro: siRNA-based downregulation of SPOP or ectopic expression of its inactive mutant forms indeed lead to decreased cell viability upon PARP inhibition with olaparib [43]. The gene discussed is PARP1; the disease is cancer.