It is biallelically inactivated in ovarian cancer; hypothesis-directed experiments have found that mutations or depletion are associated with sensitivity to radiation, platinum or PARP inhibitor treatment and it was also highlighted as a candidate gene in a hypothesis-free synthetic lethal screen approach.30,31 However, mechanistically it has been proposed to have an indirect effect on DNA repair via transcriptional regulation32 and it was recently suggested to be associated with a different pattern of genome instability than that seen in patients with BRCA mutations or BRCA1 methylation.33 The gene discussed is BRCA1; the disease is ovarian cancer.