In the mouse system, gut-derived bacterial endotoxins, such as lipopolysaccharide, have been regarded as an endogenous inducer of hepatic inflammation which exerts its effects by stimulating TNFα release from Kupffer cells, which is assumed to be a factor contributing to the progression from simple steatosis to NASH [22,23,24]. Here, TNF is linked to metabolic dysfunction-associated steatohepatitis.