Accordingly, intrahepatic gene expression and/or plasma levels of TNF-α are increased in fatty liver and in NASH patients [43] and modulation of TNF-α expression by genetic deletion or other means results in the amelioration of steatosis, inflammation, and hepatocyte damage in ob/ob mice and in dietary models of steatohepatitis [44] suggesting a pivotal role of this cytokine in NASH. This evidence concerns the gene TNF and metabolic dysfunction-associated steatohepatitis.