Haynes et al. showed that MT treatment inhibited insulin-stimulated glucose uptake by 3T3-L1 adipocytes.[39] Fu et al. reported that MT1G suppressed thyroid cancer cells by inhibiting the PI3K/Akt signaling pathway.[40] Recently, Summermatter et al. showed that suppressed expression of MT1 and MT2 genes was associated with activation of the Akt pathway, which is a crucial regulator of skeletal muscle hypertrophy, and an increase in myotube fiber size, both in vitro and in vivo. The gene discussed is INS; the disease is thyroid gland carcinoma.