Among the mechanisms directly involved between hypercortisolism and hyperglycemia, several studies have described β-cell dysfunction and reduced insulin sensitivity; impaired glucose transporter migration to the cell surface due to post-receptor defect of insulin receptor substrate-1, phosphatidylinositol-3 kinase and protein kinase B in the liver, skeletal muscle and adipose tissue; altered secretion of adipokines, such as adiponectin and leptin, leading to impaired insulin sensitivity [41]. The gene discussed is INS; the disease is Hyperglycemia.