In response to ROS, oxidation of the IκB kinase (IKK) complex occurs, leading to the release of nuclear factor kappa B (NF-κB) (46) which promotes the transcription of various pro-inflammatory mediators of endothelial dysfunction including intracellular adhesion molecule 1 (ICAM-1), the vascular cell adhesion molecule 1 (VCAM-1) and inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α (47). This evidence concerns the gene VCAM1 and endothelial dysfunction.