The study investigates the role of *BRCA1* in homologous recombination (HR) and nonhomologous end joining (NHEJ) pathways of DNA double-strand break (DSB) repair. The researchers found that *BRCA1*-deficient mouse embryonic stem (ES) cells exhibit impaired HR, as evidenced by reduced efficiency in gene targeting and altered DSB repair patterns. Specifically, *BRCA1*-deficient cells showed a 53-fold decrease in gene targeting efficiency compared to wild-type cells, and a 5- to 6-fold reduction in HR events. In contrast, NHEJ was not significantly affected in *BRCA1*-deficient cells. The results suggest that *BRCA1* plays a caretaker role in maintaining genomic integrity by promoting HR and limiting mutagenic NHEJ processes. This finding supports the hypothesis that *BRCA1* mutations contribute to the high risk of breast and ovarian cancers by disrupting HR and leading to genomic instability.The study investigates the role of *BRCA1* in homologous recombination (HR) and nonhomologous end joining (NHEJ) pathways of DNA double-strand break (DSB) repair. The researchers found that *BRCA1*-deficient mouse embryonic stem (ES) cells exhibit impaired HR, as evidenced by reduced efficiency in gene targeting and altered DSB repair patterns. Specifically, *BRCA1*-deficient cells showed a 53-fold decrease in gene targeting efficiency compared to wild-type cells, and a 5- to 6-fold reduction in HR events. In contrast, NHEJ was not significantly affected in *BRCA1*-deficient cells. The results suggest that *BRCA1* plays a caretaker role in maintaining genomic integrity by promoting HR and limiting mutagenic NHEJ processes. This finding supports the hypothesis that *BRCA1* mutations contribute to the high risk of breast and ovarian cancers by disrupting HR and leading to genomic instability.