Moreover, while prolonged iNOS blockade induces renal, heart or liver fibrosis in rodents (21–23), NO has shown proper antifibrotic roles, through the inhibition of myofibroblast activation, the abrogation of TGFβ pathway and the activation of MMP and hepatocyte growth factor (HGF), leading to less collagen deposition in other models (13, 20, 24). The gene discussed is TGFB1; the disease is Hepatic fibrosis.