Recent advances in our understanding of the molecular alterations responsible for thyroid carcinogenesis provide compelling evidence for the crucial role of mutational or non mutational abnormalities in components of survival-signaling cascades, such as TSH-R, MAPK, PI3-K/AKT, mTOR, and the IGF pathways [41] (see Table 1). This evidence concerns the gene IGF1 and thyroid gland disorder.