eNOS) inhibition has been shown to be dependent upon protein phosphatase 2A (PP2A), β2-GPI, and apolipoprotein E receptor 2 [6], however, other mechanisms have been described such as Asymmetric Dimethylarginine-mediated eNOS inhibition or impaired paraoxonase activity leading to oxidative stress and endothelial dysfunction [12,13,14]. This evidence concerns the gene APOH and endothelial dysfunction.