Activation of β-catenin, a Wnt signaling component, due either to loss of the adenomatous polyposis coli (APC) gene or to stabilization mutations in β-catenin itself results in loss of normal rhythm of crypt-villi dynamics, uncontrolled IEC proliferation, and aberrant crypt foci (ACF) formation described as precursors of intestinal adenoma and adenocarcinoma in animal models and human [15]–[17]. Here, APC is linked to adenocarcinoma.