Thus, deletion of NRF2 was found to result in rapid progression of steatohepatitis in high-fat diet fed mice (4, 5), while activation of NRF2 with sulforaphane led to reduced hepatic glucose production and improved glucose control in patients with type 2 diabetes, one of the major metabolic diseases associated with NASH (6). This evidence concerns the gene NFE2L2 and metabolic dysfunction-associated steatohepatitis.