A prominent role for β-cateninTCF7L2-dependent Wnt signaling is now acknowledged after the reports that GSK-3β overexpression in mice induces beta cell mass restriction and the development of diabetes [63], that genetic disruption of GSK-3β in beta-cells results in increased beta-cell mass and that beta-cell regeneration can be promoted by systemic administration of GSK-3β inhibitors to streptozotocin-induced neonatal diabetic rats [64]. Here, GSK3B is linked to diabetes mellitus.