In the absence of ligands binding, TSHR activation mutations could autonomously activate AC-cAMP pathway, leading to proliferation and hyperfunction of thyroid cells, thereby causing autonomic hyperfunctional thyroid adenoma, non-autoimmune hyperthyroidism, etc.[2] The TSHR loss-of-function mutations are inactivation mutations, which leads to the reduction of TSHR function such as the expression of mut receptor on eukaryotic cell membrane, the ability of binding to TSH and the activity of activating AC, thus causing hyperthyroxemia and congenital hypothyroidism.[3]. This evidence concerns the gene TSHR and Graves disease.