Endothelial dysfunction, according to current knowledge, is linked to oxidative stress, decreased nitric oxide bioavailability, increased anticoagulant properties and platelet aggregation, increased expression of adhesion molecules (such as P- and E-selectin, intercellular adhesion molecule-1 (ICAM-1), and leukocyte adhesion molecules, such as vascular cell adhesion molecule-1 (VCAM-1), increased expression of pro-inflammatory chemokines (i.e. IL-1b). This evidence concerns the gene OCA2 and endothelial dysfunction.