During DNA double-strand breaks (DSBs), BRCA1 recruits PALB2, which subsequently binds to BRCA2. This binding localizes BRCA2 and radiation-sensitive protein 51 (RAD51) to damaged DNA sites, facilitating recombination repair, thereby contributing to the preservation of genome integrity and the suppression of cancer development (Xia et al. 2006; Zhang et al. 2009; Sy et al. 2009; Buisson et al. 2010). The gene discussed is BRCA2; the disease is cancer.