The determinant role of this TLR4-LPS interaction and downstream signalling in NAFLD pathogenesis has been documented in TLR4 mutant mice in which, besides the presence of similar plasmatic levels of LPS compared to wild type animals, the expression of proinflammatory cytokines was suppressed and neither NAFLD nor insulin resistance was developed [70, 88]. The gene discussed is TLR4; the disease is Insulin resistance.