Activation of hepatic stellate cells (HSCs) plays a critical role in liver fibrosis and is characterized by the conversion from vitamin A-storing cell into myofibroblast that expresses excess profibrogenic genes, such as alpha-smooth muscle actin (α-SMA), collagen type I alpha 1 chain (Col1a1), collagen type I alpha 2 chain (Col1a2), tissue inhibitor of metalloproteinase 1 (Timp1), and fibronectin 1 (Fn1). The gene discussed is TIMP1; the disease is Hepatic fibrosis.