An observation in vitro also indicated that the eNOS Glu298Asp variant alters caveolar localization in the microdomain of endothelial cells and function deficit in this eNOS corresponding enzyme casually linking Cav-1 highlights the relevance of interaction between eNOS and Cav-1 in reducing vasoprotection in arterial disease [43]. The gene discussed is CAV1; the disease is arterial disorder.