More importantly, the finding that the decrease in the level of GSK3β in the atrium reported here is sufficient to reverse the effects of hypoinsulinemia on parasympathetic dysfunction and expression of GIRK1/GIRK4 strongly supports the conclusion that levels of this enzyme are limiting in the atrium and directly establish a role for hyperactivity of GSK3β in the pathogenesis of autonomic dysfunction in this mouse model for type 1 diabetes. The gene discussed is KCNJ3; the disease is type 1 diabetes mellitus.