Inflammatory activation of endothelial cells by cytokines such as tumor necrosis factor (TNF)-α, IL-1α or IL-1β results in the increased expression of selectins and adhesion molecules augmenting an adherence of monocytes, reduced circulation of endothelial progenitor cells, dysregulated production and bioavailability of myocardial nitric oxide, augmented oxidative stress, and increased production of procoagulant mediators, which all aggravate endothelial dysfunction and predispose to atherothrombosis [15,16,27,28]. This evidence concerns the gene TNF and endothelial dysfunction.