CRP induces complement activation, increases the uptake and oxidation of LDL-C, decreases nitric oxide production, induces tissue factor production, upregulates adhesion molecule expression, inhibits fibrinolysis through increased plasminogen activator inhibitor-1 expression, and promotes monocyte infiltration into the vascular wall, thereby playing an important role in atherosclerosis and CHD; furthermore, increased CRP is associated with metabolic syndrome, type 2 diabetes, and insulin resistance, and it is suggested to be an independent predictor of CVD in healthy individuals [19, 31]. This evidence concerns the gene CRP and metabolic syndrome.