Atherosclerosis previously defined as an obstructive disease leads to fatty deposits in the arterial wall. Nowadays, according to the best of our knowledge, specific cells, molecular mechanisms, and genes play crucial roles in the pathogenesis of the disease. Inflammatory reaction contributes to atherosclerotic lesion formation, since fatty streak leads to a plaque erosion or rupture. Experimental and clinical studies have shown that besides well-known risk factors, such as smoking,

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... , diabetes, and dyslipidemia, genetic variations in certain locuses affect the disease burden. A common genetic variability at the apoE locus has been shown to be associated with a risk for cardiovascular disease. In many studies, a higher cardiovascular risk has been associated with the presence of the apo ε4 allele, whereas the apo ε2 allele has been protective. Recent studies stated that pro-inflammatory cytokines increase the binding of low-density lipoprotein (LDL) to endothelium and smooth muscle cells, so inflammatory response solely increases lipoprotein accumulation within the vessel wall. As a conclusion, cholesterol accumulation leads to atherosclerotic plaque via several mechanisms. Genetic predisposition and inflammatory process may affect disease severity.