Remarkably, the lesions of Apcmin/+Vdr−/− mice showed higher β-catenin nuclear levels and expression of its targets genes Ccnd1/Cyclin D1 and Lef1 than those of Apcmin/+Vdr+/+ mice, suggesting that Vdr deletion promotes intestinal tumor growth through the activation of the Wnt/β-catenin pathway [40,82]. The gene discussed is VDR; the disease is intestinal neoplasm.