Genetic deletion of eNOS or over expression of caveolin-1, an endogenous inhibitor of eNOS, has been shown to cause increased leukocyte adhesion and macrophage infiltration, and accelerated atherosclerosis in apolipoprotein E (apoE) deficient mice (Sasaki et al., 2003; Fernandez-Hernando et al., 2009; Atochin and Huang, 2010; Fritzsche et al., 2010; Ponnuswamy et al., 2012). Here, NOS3 is linked to atherosclerosis.