This potentiates thrombus formation and further increases in proinflammatory cytokines [i.e., interleukins (IL-6 and IL-8, TNF-α, and monocyte chemoattractant protein 1 (MCP-1)], and expression of vascular adhesion molecules triggering endothelial dysfunction [48]. The gene discussed is CCL2; the disease is endothelial dysfunction.