CRP is also postulated to directly influence vascular vulnerability and progression of atherosclerosis through several mechanisms, including enhanced expression of local adhesion molecules, increased expression of endothelial plasminogen activator inhibitor 1 (PAI-1), reduced endothelial nitric oxide bioactivity, altered low-density lipoprotein (LDL) uptake by macrophages, and colocalization with complement within atherosclerotic lesions [9, 10, 35]. The gene discussed is SERPINE1; the disease is atherosclerosis.