For example, enhanced production in metabolic syndrome of 20-hydroxy-5,8,11,14-eicosatetraenoic acid (20-HETE) by the cytochrome P450 system and its cyclooxygenase-2-derived product 20-OH-PGE2 act to bias MSCs toward adipogenic differentiation through up-regulation of PPARγ and β-catenin, resulting in compounded inflammation-driven adipogenesis and impaired peripheral tissue maintenance through loss of otherwise uncommitted progenitors in patients with these disorders [136,137,138]. The gene discussed is PPARG; the disease is metabolic syndrome.