Fu et al. revealed in-depth molecular mechanisms of MT1G as a tumor suppressor in thyroid carcinogenesis, which involved the inhibition of cell growth and invasion and induction of cell cycle arrest and apoptosis via the inhibition of the phosphorylation of Akt and Rb, that is, through modulation of the phosphatidylinositol 3-kinase (PI3K)/AKT and Rb/E2F signaling pathways [89]. This evidence concerns the gene AKT1 and thyroiditis.