This is of clinical interest, because it is tightly associated with metabolic syndrome.14 Mice lacking STAT5 or the GH receptor (GHR) in the liver acquire characteristics of GH resistance and develop steatosis and insulin resistance.3, 4 Importantly, hepatic STAT5 deficiency contributes to CCl4−induced liver fibrosis and HCC development.15 Furthermore, hepatocyte-specific deletion of JAK2 also results in GH resistance and the development of hepatic steatosis. This evidence concerns the gene GHR and fatty liver disease.