In addition, TNF-α produces insulin resistance in skeletal muscle through the activation of κB kinase inhibitors in a p38-MAPK-dependent manner, which produces serine phosphorylation in the insulin receptor and IRS-1, and thus prevents insulin from inducing tyrosine phosphorylation and impairs the corresponding activation of the PI3 kinase and Akt [80]. This evidence concerns the gene INS and Insulin resistance.