Therefore, attempts to correct the relative lack of BH4 by supplementing BH4 to prevent uncoupling of eNOS and maintain endothelial function have been reported in several diseases such as patients of coronary risk factors, HT, DM, and ischemia reperfusion (Heitzer et al., 2000; Mayahi et al., 2007; Porkert et al., 2008). The gene discussed is NOS3; the disease is hematocrit.