Moreover, as our thyroid damage model should induce metabolic changes, the increase of TNF-α is in agreement with the theory where TNF-α may promote atherogenesis through (1) down-regulation of ApoE secretion, which is an important agent in the lipoprotein metabolism; (2) stimulation of vascular cells calcification; and (3) the endothelial dysfunction increase. Here, APOE is linked to thyroiditis.