The pathophysiology of this autoimmune disease involves multiple regulatory mechanisms including regulatory T cell failure, proliferation of autoreactive T and B cells, increased Human Leukocyte Antigen D affinity for the TSH receptor, leading to more efficient antigen presentation, or the presence of a more immunogenic TSH receptor haplotype or increased exposure to the TSH receptor peptide [18,19]. The gene discussed is TSHR; the disease is autoimmune disease.