Hence, we sought to investigate the role of N-RAS in fibrotic liver disease by using mice deficient for N-RAS and well-established experimental hepatotoxic models (carbon tetrachloride, CCl4 and bile duct ligation, BDL) [9, 10]; in combination with analyses of N-RAS expression in chronic liver disease patients with distinct degree of fibrosis. The gene discussed is NRAS; the disease is liver disorder.