Given that neither PALB2 nor BARD1 were altered at a sufficient frequency in the PROfound or TRITON2 trials to reliably determine the impact of each gene on PARP inhibitor sensitivity, these functional data fill an important gap by providing direct evidence that loss of PALB2 or BARD1 is sufficient to confer an HR-deficient phenotype in prostate cancer cells and suggest that alterations in PALB2 or BARD1 may be sufficient to drive PARP inhibitor sensitivity in mCRPC. This evidence concerns the gene PALB2 and prostate carcinoma.