While in HT the autoimmune processes lead to apoptosis and destruction of the thyroid follicles, and subsequently hypothyroidism, in GD the immune-mediated activation of TSHR-reactive B cells results in the production of stimulating TSHR antibodies which in turn induce thyroid cell proliferation and function, manifested as hyperthyroidism (1, 2). The gene discussed is TSHR; the disease is hyperthyroidism.