Abstract: Non-alcoholic steatohepatitis (NASH) has a high risk to develop liver fibrosis, which is a key factor of liver complications in NASH patients. The severity of liver fibrosis directly affects the patient's quality of life and long-term survival. Currently ongoing or completed phase III clinical trials of NASH treatments use attenuation of liver fibrosis as a primary endpoint to evaluate the efficacy of medical treatment. Therefore, it is important to understand the mechanism of liver fibrosis and molecular targets for NASH treatment. The aim of this review is to provide a concise update on the pathogenesis of NASH and associated fibrotic progression, end-points of clinical trials, molecular targets and drugs under ongoing investigation.