Fourteen of 16 patients with metastatic, castration-resistant prostate cancer and genetic defects in repair of DNA damage had a response to the PARP inhibitor olaparib. Anemia and fatigue were the major toxic effects. Prostate cancer is the most common cancer in men and the sixth leading cause of death from cancer among men throughout the world. 1 The interpatient molecular heterogeneity of this disease is well recognized; however, treatment to date has not been molecularly stratified. 2 , 3 It would be useful to identify predictive biomarkers in order to provide more precise treatment for this disease. 4 Metastatic, castration-resistant prostate cancer can have genomic aberrations that interfere with DNA repair. 3 , 5 Some of these aberrations have been associated with sensitivity to platinum and poly(adenosine diphosphate ADP–ribose) polymerase (PARP) inhibitors, suggesting that treatment with a PARP inhibitor . . .