Although initially counterintuitive, the correlation between BRCA2 mutations and longer PFS in our model is consistent with two potential mechanisms: (i) adaptive silencing of the spindle assembly checkpoint (via NSFL1C/AURKB downregulation) to mitigate genomic instability, as reported in BRCA2-deficient prostate cancer (36), and (ii) enhanced tumor immunogenicity stemming from accumulated DNA damage. This evidence concerns the gene BRCA2 and prostate carcinoma.