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. Here, CYP2B6 is linked to metabolic dysfunction-associated steatotic liver disease.