As an autoimmune disease that involves differentiation of helper T lymphocyte-17 and secretion of IL-17, TED triggers a pathogenesis that leads to a notable increase in cytokines such as tumor necrosis factor-α (TNF-α), interleukins (i.e., IL-1β, IL-6, IL-13, IL-17A, IL-18), and regulated upon activation, normal T Cell expressed and presumably secreted (RANTES), etc. (43, 44), the elevation of which eventually contribute to the activity assessment of TED. This evidence concerns the gene IL17A and autoimmune disease.