A GCGR/GLP1R dual agonist Cot was utilized as it had been proved the liver effects were predominantly through GCGR, and extrahepatic improvement via GLP1R.[11] Indeed, Cot alleviated liver steatosis, showing as reduced BW, LW, LW/BW, liver TG content and morphology, as well as altered fatty acid synthesis and oxidation genes and proteins, which was in accordance with recent report.[11] Delating hepatic CD9 by AAV‐TBG‐shCD9 significantly abolished the remission of steatosis and lipid accumulation by Cot treatment, except BW (Figure 7B‐E; Figure S11, Supporting Information). This evidence concerns the gene CD9 and fatty liver disease.