Th17 cells have been demonstrated in atherosclerotic plaques and shown to exert proinflammatory effects by secreting substantial quantities of the proinflammatory cytokine interleukin 17A (IL-17A), and by promoting recruitment of pathogenic macrophages [41]; IL-17A has also been found to lead to endothelial dysfunction by activating RhoA/Rho-kinase and reducing NO bioavailability [43, 44]. This evidence concerns the gene IL17A and endothelial dysfunction.