Subsequent studies on liraglutide-treated in vitro murine and human hepatocyte models and in vivo murine models of NASH have shown that liraglutide caused a reduction in liver enzymes concentration, oxidative stress, and hepatic inflammation and steatosis by downexpression of profibrogenic genes (transforming growth factor-beta (TGF-β), collagen type I alpha 1 gene (COL1A1), collagen type I alpha 2 gene (COL1A2), collagen type III alpha 1 chain gene (COL3A1), and hepatic stellate cells activation genes (actin alpha 1, vimentin [VIM]). The gene discussed is COL1A2; the disease is steatosis.