There is evidence that T3 binding to the S1 site of the αVβ3 receptor activates PI3K (lipid kinase) and increases cellular invasiveness and metastasis, whereas the binding of T4 to the S2 site of this ERK1/2 active receptor alters FGF2 expression and promotes angiogenesis, with both these pathways favoring tumor growth. The gene discussed is MAPK3; the disease is neoplasm.