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]. Here, PALB2 is linked to prostate carcinoma.