They suggested that TSH can upregulate the TSH receptor at the mRNA level in cultured human thyroid cells,[14] and it can also suppress the expression of interferon g-induced Fas,[15] intercellular adhesion molecule (ICAM)-1,[16] and class II transactivators on the thyroid cell surface.[17] Therefore, the previous studies suspected that Fas-mediated apoptosis of thyroid cells can be induced by the rapid reduction in TSH levels that occur after tumor resection, which may activate autoimmune responses against the thyroid gland, leading to the occurrence of Graves’ disease after surgery. Here, FAS is linked to neoplasm.