Furthermore, the mechanism of palmitate-mediated ROS generation via NOX2 was demonstrated, and it was found that endocytosis of the TLR4–MD2 complex generated ROS by a MyD88/TRIF-independent in human macrophages, which might be related with pathogenesis of non-alcoholic fatty liver disease (NAFLD) in human patients [36]. Here, TLR4 is linked to metabolic dysfunction-associated steatotic liver disease.