Although the antitumour activity from PARPi is best established for prostate cancers with germline or somatic BRCA1 and BRCA2 alterations, clinical benefit also extends to other alterations in HRR genes, namely, PALB2, BRIP, FANC, RAD51B, RAD51C, RAD51D, RAD54L, CHEK2, and, to a lesser extent, ATM and CDK12 [5,6,7,8,9]. This evidence concerns the gene BRCA2 and prostate carcinoma.