Genetic deletion of eNOS or over expression of caveolin-1 has shown increased leukocyte EC interaction, aggravated infection under disease conditions, and accelerated atherosclerosis in apolipoprotein E (apoE) deficient mice (Sasaki et al., 2003; Fernández-Hernando et al., 2009, 2010; Atochin and Huang, 2010; Fritzsche et al., 2010). Here, APOE is linked to infection.