PARP inhibition has been associated with an increased number and effector function of cytotoxic T cells and NK cells, showing synergy with CTLA-4 inhibition in an immunocompetent BRCA1−/− model of ovarian cancer, with efficacy driven by improved peritoneal T cell effector function and IFNγ production with combination therapy.93 Treatment of human BRCA−/− UWB1.289 cells with IFNγ caused significantly greater cytotoxicity when the cells were treated with a PARP inhibitor,93 suggesting PARP inhibition may prime cells for IFNγ mediated cell death. The gene discussed is IFNG; the disease is ovarian carcinoma.