For example, the “just right” signaling model of Wnt/beta-catenin signaling in familial adenomatous polyposis (FAP) demonstrated a selection for genetic mutations in the APC gene that retain some of its ability to decrease β-catenin signaling levels, rather than mutations that result in complete loss of function of APC and subsequent constitutive Wnt/beta-catenin signaling [45]. This evidence concerns the gene CTNNB1 and Familial adenomatous polyposis.