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]. The gene discussed is ATM; the disease is prostate carcinoma.