The article investigates the role of the *BRCA2* gene in embryonic development and radiation sensitivity. *BRCA2* mutations are associated with early-onset breast cancer, and the gene is highly expressed in rapidly proliferating cells. The authors generated *BRCA2* knockout mice by targeting the *Brca2* locus in embryonic stem (ES) cells. These mice exhibit embryonic lethality around day 6.5 of gestation, coinciding with the onset of detectable *Brca2* expression. The knockout embryos show a developmental arrest, particularly in mesoderm formation, suggesting a role for *BRCA2* in cell proliferation. The *BRCA2* protein interacts with the DNA-repair protein Rad51, and this interaction is essential for DNA repair. Homozygous *BRCA2* and *Rad51* mutants are hypersensitive to γ-irradiation, indicating a defect in DNA repair. The authors conclude that *BRCA2* and *Rad51* likely function in similar pathways, and their interaction may explain the high penetrance of early-onset cancer in patients with *BRCA1* or *BRCA2* mutations. The study also suggests that *Rad51* could be a tumor suppressor gene, and the *BRCA2* knockout mice may serve as a model for understanding the genetic basis of breast cancer.The article investigates the role of the *BRCA2* gene in embryonic development and radiation sensitivity. *BRCA2* mutations are associated with early-onset breast cancer, and the gene is highly expressed in rapidly proliferating cells. The authors generated *BRCA2* knockout mice by targeting the *Brca2* locus in embryonic stem (ES) cells. These mice exhibit embryonic lethality around day 6.5 of gestation, coinciding with the onset of detectable *Brca2* expression. The knockout embryos show a developmental arrest, particularly in mesoderm formation, suggesting a role for *BRCA2* in cell proliferation. The *BRCA2* protein interacts with the DNA-repair protein Rad51, and this interaction is essential for DNA repair. Homozygous *BRCA2* and *Rad51* mutants are hypersensitive to γ-irradiation, indicating a defect in DNA repair. The authors conclude that *BRCA2* and *Rad51* likely function in similar pathways, and their interaction may explain the high penetrance of early-onset cancer in patients with *BRCA1* or *BRCA2* mutations. The study also suggests that *Rad51* could be a tumor suppressor gene, and the *BRCA2* knockout mice may serve as a model for understanding the genetic basis of breast cancer.