Despite the dose used in mice being well below the RP2D for rucaparib monotherapy in ovarian cancer (600 mg, resulting in a Cmax of 6 μM/l, equivalent to 100mg/kg in mice [24, 25]), this result however confirms in vivo studies of other PARP inhibitors (BMN673, olaparib) performed by Norris and by Smith from the Pediatric Preclinical Testing Program, who also failed to show any significant responses or survival benefit by single agent PARP inhibitors [26, 27]. This evidence concerns the gene PARP1 and ovarian carcinoma.