Third, the onset and progression of NASH in p62‐KO mice might be influenced by not only increased LPS production in the intestines, the disturbed phagocytotic function of KCs, but also insulin resistance and hyperleptinemia associated with obesity, and disturbed autophagy and activation of hepatic stellate cells associated with the p62 deletion. Here, TBCE is linked to metabolic dysfunction-associated steatohepatitis.