While the literature on CYP-sEH pathway association with human metabolic syndrome refers to contradictory findings39,40,42, 43, 44, 45,47,49, 50, 51, 52, 53 (e.g. changes in hepatic epoxide levels were linked to either increased or decreased CYP epoxygenase activity, depending on the stage of disease and the type of patients in MASLD/MASH),39,49 there is converging evidence suggesting that the metabolic component of obesity is characterized by reduced diols and/or sEH activity. The gene discussed is EPHX2; the disease is obesity due to melanocortin 4 receptor deficiency.