Previous studies have demonstrated that the activation of I1R may improve hypertension via sympathoinhibition [24]; the activation of I2R may improve insulin resistance via the AMP kinase pathway to enhance glucose uptake in type-2 diabetic animal models [25–27]; and the stimulation of I3R may stimulate insulin secretion from pancreatic β cells [28]. The gene discussed is NISCH; the disease is hypertensive disorder.