In DM, JNK activation generates phosphorylation of insulin receptor substrate (IRS-1) at serine residues, therefore causing insulin signal transduction to be downregulated and insulin resistance to occur, hence activating NFκB by impaired enzymatic activity in the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway. This evidence concerns the gene AKT1 and Insulin resistance.