This molecular vulnerability is further exploited by synthetic lethal inhibition of PARP1/2 with a range of PARP inhibitor (PARPi) agents as maintenance in first-line treatment, and at relapse, showing substantial benefit in patients with HR-deficient ovarian cancer due to BRCA1/2 mutations or other genetic lesions, estimated to be over 50% of HGSC2,3. The gene discussed is PARP1; the disease is ovarian carcinoma.