In addition, polyadenosine diphosphate-ribose polymerase (PARP) inhibitors were developed based on the mechanism of the homologous recombination repair defects associated with pathogenic variants in these genes.2 The target BRCA1 and BRCA2 cancer types have expanded to prostate3 and pancreatic cancers4 because pathogenic variants were enriched in these patients, and the therapeutic efficacy of PARP inhibitors in these cancers has also been shown.5,6. This evidence concerns the gene BRCA2 and cancer.