FAs themselves also promote hepatic insulin resistance via Toll-like receptor 4 (TLR4) activation that increases the release of inflammatory biomediators such as IL6, IL1β, and the TNFα receptor [7], indicating a vicious cycle of lipid accumulation, and IR as a crucial mechanism in the pathogenesis of NASH, among other mechanisms. The gene discussed is TLR4; the disease is metabolic dysfunction-associated steatohepatitis.