Given well-known examples of neoplasms arising in the setting of FAP (e.g., desmoid fibromatosis, hepatoblastoma) that occur independently from APC mutations in the sporadic setting and the established role of WNT/β-catenin signaling in osteogenesis (reviewed in [8, 9]), we set out to analyze a cohort of craniofacial osteomas for the presence of CTNNB1 gene mutations. This evidence concerns the gene FAP and desmoid tumor.