In these mouse models, improvements in liver steatosis, inflammation, and fibrogenesis were demonstrated, and are associated with the following: a decrease in alpha smooth muscle actin (αSMA) and collagen type I alpha 1 (COL1A1) expression [120]; and elevated levels of epithelial–mesenchymal transition (EMT)-promoting protein calcium-binding protein A4 (S100A4). The gene discussed is COL1A1; the disease is Hepatic steatosis.