It is believed that in the pathological conditions (e.g., obesity), leptin accelerates the development of atherosclerosis by several mechanisms: increasing synthesis of proinflammatory cytokines in macrophages and monocytes (IL6, IL12, IL18, and TNFα), enhancing expression of endothelin 1, intensifying oxidative stress in endothelial cells, promoting migration and proliferation of the vascular smooth muscle cell, and stimulating platelet aggregation [16]. This evidence concerns the gene LEP and atherosclerosis.