CTNNB1 and Familial adenomatous polyposis: With respect to the underlying mechanism of DF, the constitutive activation caused by the mutation of the β-catenin oncogene CTNNB1 (in sporadic cases) (23) or the germline activation of the adenomatous polyposis coli (APC) gene (in FAP patients) (24) will activate the Wnt pathway, thus preventing the degradation of cytosolic β-catenin.