BRCA2 is a critical DNA repair protein that functions primarily in homologous recombination-mediated double-strand break repair 1. Mechanistically, BRCA2 binds RAD51 and promotes its assembly onto single-stranded DNA, targeting RAD51 to ssDNA over double-stranded DNA and stabilizing RAD51-ssDNA filaments by blocking ATP hydrolysis. BRCA2 also participates in R-loop management through interaction with the TREX-2 complex, preventing transcription-associated genomic instability independently of its homologous recombination role. Additionally, BRCA2 regulates centrosome duplication in concert with NPM1. Germline BRCA2 mutations substantially increase breast cancer susceptibility, with premenopausal women carrying pathogenic variants experiencing a 27% cumulative incidence of contralateral breast cancer at 10 years 2. BRCA2 mutations also predispose to ovarian, pancreatic, gastric, thyroid, laryngeal, and prostate cancers 1. Notably, BRCA2-deficient tumors demonstrate enhanced immunogenicity and superior response to immune checkpoint blockade compared to BRCA1-deficient tumors, with enriched adaptive and innate immune gene expression programs 3. Clinically, MRI surveillance significantly reduces breast cancer mortality in BRCA1-variant carriers (HR: 0.20) 4, though benefits remain unclear for BRCA2 carriers. Genetic testing for BRCA mutations in high-grade prostate cancer enables family screening and personalized cancer prevention strategies 5.