Under conditions of chronic inflammation, sustained activation of ECs by inflammatory stimuli, such as interleukin (IL)-6, tumor necrosis factor-α (TNF-α), IL-1β, and pathogens, cause alterations in normal endothelial function, resulting in impaired endothelial-dependent immune response, which is the hallmark of endothelial dysfunction (6–9). This evidence concerns the gene IL1B and endothelial dysfunction.