As a pre-dispositional factor in atherosclerosis, leukocyte-endothelial adhesion is known to initiate endothelial dysfunction, followed by increased expressions of pro-inflammatory cytokines including tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6) and monocyte chemoattractant protein-1 (MCP-1) [18–20]. This evidence concerns the gene IL6 and endothelial dysfunction.