In agreement with our findings, Gurses et al. [16] observed a shift to pro-inflammatory M1-macrophage phenotype in EAT of patients with coronary artery disease (CAD) compared to the control group (without CAD), reflected by increased of CD11c, CD11c/CD68 and CD11c/CD206 ratios, but not CD206. According to our results, Hirata et al. [17] showed similar results, demonstrated that pro-inflammatory macrophages are more dominant in EAT when compared with and without CAD patients. This evidence concerns the gene CD68 and coronary artery disorder.