Graves disease is an autoimmune disorder in which antibodies to the thyroid-stimulating hormone receptors (TSHR) are formed by the patient's body, and therefore, resulting in hyperthyroidism. As the antibodies bind to the TSHR, these receptors will be activated causing abnormal growing of the thyroid gland and excessive production of thyroid hormone (thyrotoxicosis).

Susceptibility to Graves disease is found to be associated with the human leukocyte antigen (HLA) alleles, however, HLA haplotypes vary among the different ethnic groups. Genetic studies have shown that polymorphisms in the cytotoxic T-lymphocyte antigen 4 (CTLA-4) gene have a role in causing the symptoms of Graves disease. In addition, alterations in the vitamin D-binding protein (DBP) gene may increase the susceptibility to Graves disease.