In our study, disrupting association between SMAD4 and SMAD3 by RGS6 partially blocked nuclear translocation of SMAD3 and did not prevent dephosphorylation of p-SMAD3 in the presence of TβRI inhibitor, suggesting that in NSCLC cells, nuclear entry of p-SMAD3 in response to TGF-β treatment occurs via both SMAD4-dependent and -independent mechanisms. The gene discussed is SMAD3; the disease is non-small cell lung carcinoma.