Collectively, these findings indicate that chronically elevated ET-1 levels could play a fundamental role in the development of IR and glucose intolerance; however, it remains unclear whether ET-1 is involved in the development of metabolic impairments associated with IH and OSA and whether pharmacological treatment with ET-1 receptor antagonists would provide metabolic benefit in these subjects. The gene discussed is EDN1; the disease is isolated hemihyperplasia.