Several hypotheses have been proposed to explain the worse outcomes of patients with clinical and subclinical PAD compared to those without: (1) the increased atherosclerotic burden in PAD patients [4]; (2) the higher prevalence of left main and multivessel coronary artery disease in these patients [5]; (3) the higher levels of C-reactive protein, homocysteine or amyloid A, as markers of inflammation and (4) the rates of poorly controlled diabetes and time-dependent tobacco exposure, which are significantly higher in PAD patients [6,7]. This evidence concerns the gene CRP and peripheral arterial disease.