The increased WWI may reflect a state of adipose tissue dysfunction, which produces a variety of proinflammatory cytokines and adipocytokines such as interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and resistin, leading to inflammatory response, endothelial dysfunction, insulin resistance (IR), and ultimately atherosclerosis and arterial calcification (32–34). This evidence concerns the gene RETN and endothelial dysfunction.