To clarify these conflicting functional results, we sought to determine the relative contribution of Tcf7l2 in beta cells to the T2D phenotypes seen in mice overexpressing Tcf7l2. Toward that, we engineered mice with Tcf7l2 expression restored to endogenous baseline levels in beta cells while maintaining overexpression in peripheral metabolic tissues where Tcf7l2 is normally expressed, including brain, liver, gut and fat. The gene discussed is TCF7L2; the disease is type 2 diabetes mellitus.