The evidence for these suppositions includes the fact that relative to control cEAT, there was significant up-regulation in atherosclerotic cEAT of pro-inflammatory 11βHSD-1, CCL19, CCL21 and PGD2S; gp91phox [NADPH oxidase], a major source of vascular ROS; VEGF and VEGFGR1, which partake in vasa vasorum neogenesis and angiotensinogen, which promotes endothelial dysfunction and vasoconstriction. This evidence concerns the gene FMO5 and endothelial dysfunction.