Several mechanisms have been proposed: (1) autoimmune inflammation mediated by thyroid autoantibodies (e.g., thyroid-stimulating immunoglobulins (TSI), anti-thyroid peroxidase (anti-TPO)), (2) direct effects of thyrotoxicosis on cardiac and pericardial tissues, and (3) increased capillary permeability [9]. The gene discussed is TPO; the disease is thyrotoxicosis.