Aberrant activation of this pathway, such as through mutations in the adenomatous polyposis coli (APC) gene, can result in excessive β-catenin accumulation and has been implicated in the pathogenesis of several cancers, including colorectal carcinoma.204 Although less studied in periodontitis, emerging evidence suggests that dysregulation of Wnt/β-catenin signaling may contribute to the imbalance between bone resorption and formation in periodontal disease.205–208. The gene discussed is APC; the disease is cancer.