Interestingly, we found that knockdown of either TβRII or Smad4 attenuated TGF-β-induced nuclear accumulation of p-Smad3L suggesting that the tumor-promoting activity of autocrine TGF-β is likely mediated in part by its stimulation of linker region phosphorylation of Smad3. The gene discussed is TGFBR2; the disease is neoplasm.