Pathological activation and signaling of toll-like receptor 4 (TLR4) by non-immune ligands (including FFAs) and immune ligands (including gut-derived lipopolysaccharide or LPS) contribute to the inflammation present in NAFLD (Lu et al. 2008, Broering et al. 2011). This evidence concerns the gene TLR4 and metabolic dysfunction-associated steatotic liver disease.