In opposition to the enhanced production of 20-HETE by the cytochrome P450 system observed in metabolic syndrome, MSCs generate P450-derived epoxyeicosatrienoic acids (EETs) from arachidonic acids, and when administered exogenously these lipid mediators have been shown to decrease adipocyte differentiation of MSCs via an increase in heme oxygenase-1 and decrease in PPARγ, C/EBPα, and Fas and to reprogram adipocyte stem cells to a new phenotype displaying a smaller cell size, increased secretion of adiponectin, and decreased secretion of inflammatory cytokines [282]. This evidence concerns the gene ADIPOQ and metabolic syndrome.