As far as the molecular mechanisms, patients with AD have been found to have increased levels of atherosclerosis markers, including fractalkine, chemokines (e.g., CCL4, CCL17, CCL28, CXCL5, CXCL10), hepatocyte growth factor (HGF), as well as increased levels of mediators of atherosclerosis, such as E-selectin or PI3/elafin, IL-16, and IL-20, which are proportional to the extension or cutaneous disease [39]. The gene discussed is CXCL5; the disease is atherosclerosis.