Nonalcoholic fatty liver disease (NAFLD) is a chronic liver disease with high incidence. NAFLD is closely related to obesity, diabetes, hyperlipidemia and other metabolic syndromes, and it is one of the important public health problems at present. Its specific pathogenesis is still unclear. At present, some studies believe that ferroptosis is involved in the occurrence and development of NAFLD, and ferroptosis is a new type of programmed cell death. Nrf2 is an important nuclear factor in the regulation of ferroptosis. First of all, Nrf2 can directly or indirectly regulate the downstream antioxidant GPX4 to participate in ferroptosis and the development of NAFLD, and can stimulate FSP1 transcription or directly stimulate HO-1 and Sesn2 transcription to play an antioxidant role when GPX4 is inactivated. Secondly, iron overload is closely related to ferroptosis and NAFLD. Nrf2 may reduce ferroptosis caused by iron overload by controlling iron storage and iron output, and finally improve NAFLD. However, the current research focuses on Nrf2 regulating iron storage affecting NAFLD, while Nrf2 regulating iron output and affecting ferroptosis and NAFLD have not been reported. In addition, Nrf2 is expected to regulate lipid peroxidation and inhibit ferroptosis by directly affecting PPARγ or indirectly affecting AMPK. Finally, the study shows that activating Nrf2 may inhibit ferroptosis by regulating mitochondrial dysfunction. All in all, Nrf2 can participate in the occurrence and development of ferroptosis and NAFLD through many ways. It is hoped that more ways related to Nrf2 will be found in the future to help improve NAFLD.