To resolve this issue and to further define the role of CYP4A genes in production of ROS during hepatic steatosis, mouse models overexpressing CYP4A10 and CYP4A14 will be needed to determine if excessive fatty acid induces uncoupling of the P450 catalytic cycle and generation of ROS during the progression of NAFLD to NASH. This evidence concerns the gene CYP2B6 and metabolic dysfunction-associated steatohepatitis.