Nonalcoholic fatty liver disease (NAFLD) is a common chronic liver disease, which might develop into nonalcoholic steatohepatitis (NASH), liver cirrhosis and even carcinoma without effective management. Necroptosis mediated by receptor interacting protein kinase (RIPK) is a novel type of programmed cell death discovered in recent years, which can eventually lead to cell membrane lysis and inflammation. As an important sensor of intracellular and extracellular stress, the RIPK family induces and regulates the activation of necroptosis, and is involved in inflammation and other immune responses. In recent years, studies have shown that RIPK-regulated necroptosis plays an important role in the development of NAFLD. In animal NAFLD/NASH model, the expression of RIPK is related to the degree of hepatic steatosis. In some clinical studies, it was also observed that RIPK expression levels were elevated in NAFLD/NASH patients compared with healthy controls. However, whether necroptosis is a factor which a celerates the progression of liver disease, or a protective factor in the development of liver disease, is still inconclusive. Some studies have shown that RIPK inhibitors may provide guidance for NAFLD treatment. This review provides the molecular mechanisms of necroptosis and its relationship with NAFLD, introduces the important role of RIPK, and summarizes its research progress in the treatment of NAFLD, providing a theoretical basis for further exploration of its mechanism and new treatments for NAFLD.