Without H4B, eNOS may become uncoupled and cannot function properly, while the presence of H4B stabilizes human eNOS both in vitro and in vivo (Rodriguez-Crespo et al.1997); the addition of H4B to the cultured cell or experimental animal elevates accumulated eNOS protein level and biological NO amount and improves endothelial dysfunction, hypertensive diastolic dysfunction, ischemia-reperfusion injury, myocardial infarction and diabetic nephropathy conditions (Faria et al.2012; Roe and Ren 2012). This evidence concerns the gene NOS3 and endothelial dysfunction.