Higher levels of VCAM-1, ICAM-1, and E-Selectin in SCD patients are usually coupled with significantly low plasma NO levels, derived from the stimulating action of various biological modifiers such as hypoxia, thrombin, and cytokines on the normally quiescent endothelium [19], as well as from the pro-inflammatory effects of reperfusion-injury physiology [21,22]. This evidence concerns the gene VCAM1 and Schnyder corneal dystrophy.