We observed that hepatic TM4SF5 overexpression caused more food intake during the daytime, increased apelin production, and higher plasma and hepatic lipid levels, eventually leading to peroxisomal β-oxidation, mTOR activation, and autophagy inhibition, which are processes that may contribute to the development of earlier phenotypes for NASH. The gene discussed is MTOR; the disease is metabolic dysfunction-associated steatohepatitis.