In all of these studies, there was a decrease in the phosphorylation of the insulin receptor (36), insulin receptor substrate 1 (IRS-1) (37), and serine/threonine protein kinase B (Akt) activity (38), and an increase in the phosphorylation of protein tyrosine phosphatase 1B (39), indicating that the insulin signal is impaired due to post-receptor effects, which have been suggested to contribute to neural insulin resistance by dephosphorylating upstream insulin cascade components. The gene discussed is AKT1; the disease is Insulin resistance.