We showed that hepatic Chrebpa is reduced in several mouse liver fibrosis (CCl4, TAA, and BDL) models and human liver fibrosis due to HBV, NASH, alcohol liver disease, and primary biliary cholangitis.[15, 16, 17, 18] We also identified Chrebpα as a previously unknown downstream target of TGFβ signaling in hepatocytes. This evidence concerns the gene TGFB1 and metabolic dysfunction-associated steatohepatitis.