In addition to its role in the pathogenesis of atherosclerosis and CAD40,41, a-FABP has also been shown to contribute to microvascular or endothelial dysfunction by stimulating fatty acid-mediated endothelial toxicity through multifaceted mechanisms related to obesity and metabolic disorders; these may include diminished endothelial nitric oxide synthase (eNOs) production, oxidative stress, pro-inflammatory cytokine secretion, and the activation of the renin-angiotensin system and apoptosis42,43. This evidence concerns the gene NOS3 and atherosclerosis.