For example, while altered Fas expression and downregulation of anti-apoptotic Bcl-2 genes has been implicated in increased thyrocyte death seen in Hashimoto’s thyroiditis, it has been suggested that TSH-mimicking TSH receptor antibodies in Graves’ disease inhibit Fas expression, thereby promoting anti-apoptotic mechanisms resulting in goiter formation and inducing death of intrathyroidal lymphocytes instead [32,36]. The gene discussed is BCL2; the disease is goiter.