Approximately 50% of high‐grade serous ovarian cancers (HGSOCs) are deficient in HR because of germline or somatic mutations in BRCA1/2 (20%), the epigenetic silencing of BRCA1 (11%), the amplification or mutation of EMSY (8%), the deletion of PTEN (7%), the hypermethylation of RAD51C (3%), mutations in ATM or ATR (2%) or mutations in Fanconi anemia genes (5%).36 The key genes and modulators of the HR pathway that might induce synthetic lethality with PARP inhibitors are under investigation. This evidence concerns the gene RAD51C and ovarian serous adenocarcinoma.