Studies on the molecular mechanisms of thyroid hormone action and in the development and course of cancer have indicated a route of gene action, in which the pro-hormone thyroxine (T4) acts via integrin αvβ3, MAPK signaling, and ERK mitogen (1/2-protein kinase and extracellular signal-regulated kinase 1/2), mediated by phosphorylation of the thyroid β1 receptor (TRβ1), thereby inducing angiogenesis and tumor proliferation (Bergh et al., 2005). Here, TG is linked to neoplasm.