The role of CYP2E1 in NASH pathogenesis is supported in vitro via the impact of CYP2E1-derived ROS on stellate cell activation [50], by results of overexpression of CYP2E1 in mice [51] and in mice fed a high-fat diet [52]. This evidence concerns the gene CYP2E1 and metabolic dysfunction-associated steatohepatitis.