Non-alcoholic fatty liver disease (NAFLD) is a kind of metabolic disorder characterized by excessive fat deposition in the liver and ranging from simple steatosis (simple NAFLD) to nonalcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma [1]. It has recently been increasing annually; for example, it was recently estimated to have a global prevalence of 32.4%, which seriously threatens human health [2]. Thus, the discovery of new therapeutic targets is of great importance because there is no specified drug for the treatment of NAFLD. On the other hand, the pathogenesis of NAFLD is complicated and still unclear. Recent studies have proposed ferroptosis as related to the disease progressions of NAFLD. Preliminary evidence indicated that ferroptosis in hepatocytes and hepatic macrophages could induce NASH and that complex regulatory mechanisms were involved. In the future, inhibition of ferroptosis may hopefully become an emerging target in treating NAFLD.