Pathophysiologically, PAD is related to endothelial damage and the triggering of inflammatory mediators such as IL-1β; followed by continuous attempts of endothelial regeneration denoted by the release of molecules such as ICAM-1 (Intercellular Adhesion Molecule 1) and VEGFR (Vascular Endothelial Growth Factor Receptor) [1,2,14]. The gene discussed is ICAM1; the disease is peripheral arterial disease.