This combination of increases in intestinal permeability and plasma LPS levels induce the production of pro-inflammatory cytokines (ILs, TNF-α) and CRP that can in turn induce the serine phosphorylation of insulin receptor substrate-1, leading to insulin resistance (Hotamisligil, 2006; Hotamisligil and Erbay, 2008). The gene discussed is TNF; the disease is Insulin resistance.