This correlation is supported by several potential mechanisms, including decreased NO bioavailability and production by endothelial cells resulting in endothelial dysfunction [32], increased matrix metalloproteinase activity from leukocytes leading to elastin fiber degradation within the arterial wall [33], increased bioapatite production from VSMCs contributing to arterial wall calcification [34], and the upregulation of glycosaminoglycans (such as decorin, versican, biglycan, and hyaluronan) that reinforce arterial stiffness [35,36]. The gene discussed is ELN; the disease is endothelial dysfunction.