This process may occur through the contribution of NAFLD per se to systemic and hepatic insulin resistance and/or through the systemic release of several pathogenic mediators from the steatotic and inflamed liver, such as increased reactive oxygen species, advanced glycation end products, C-reactive protein, plasminogen activator inhibitor-1, transforming growth factor-beta and other pro-inflammatory, pro-coagulant and pro-fibrogenic factors. The gene discussed is CRP; the disease is Insulin resistance.