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The tumor suppressor genes breast cancer 1 (BRCA1) and breast cancer 2 (BRCA2) are key players in DNA damage response and homologous recombination (HR), which are critical for the repair of DNA double-strand breaks to maintain the fidelity of the genome. Mutations in BRCA1/BRCA2 lead to genetic instability and frequently cause familial breast and ovarian cancers [12]. While little is known about how these tumor suppressor genes affect craniofacial development, a recent study has shown that non-syndromic cleft lip and palate, one of the most common human craniofacial deformities, are associated with dysregulation of the gene regulatory network via BRCA1 [13]. Since germline mutations in DNA repair genes have been linked to congenital defects [8], it is tempting to hypothesize that the BRCA1/BRCA2-dependent DNA damage and repair machinery is critical for the prevention of craniofacial abnormalities. Therefore, it is important to understand how BRCA1/BRCA2 function in CNCCs during craniofacial development. 2ff7e9595c