It has been proven that the reduced eNOS/NO activity activates NF-κB responsible for the expression of endothelin-1 and other proinflammatory mediators including TNF-α, interleukin 6 (IL-6), free radicals, chemokines, and adhesives molecules (ICAM-1, endothelial leucocyte adhesion molecule-1 (ELAM-1)), as well as inducible NO synthase (iNOS) contributing to endothelial dysfunction. The gene discussed is SELE; the disease is endothelial dysfunction.