We and others demonstrated that diabetic conditions, which are usually associated with increased TGF-β levels, induce PI3 K and Akt activation, leading to FoxO3a phosphorylation and its nuclear exclusion and inactivation in both streptozotocin-induced type 1 diabetes and type 2 diabetic db/db mice [2, 30]. The gene discussed is AKT1; the disease is type 1 diabetes mellitus.