However, this model had various limitations, including (i) BRAFV600E was expressed in all thyroid cells from the fetal period, suggesting that this is a model of hereditary rather than sporadic thyroid cancers; (ii) serum TSH levels were elevated by BRAFV600E-mediated suppression of thyroid function, which by itself can induce thyroid goiters and sometimes tumors; and (iii) BRAFV600E expression was controlled by the Tg promotor rather than the original Braf promoter [3]. Here, BRAF is linked to thyroid gland carcinoma.