It is tempting to extrapolate from our results on the normal mammary epithelium to suggest that Smad2 might be a better molecular target than TGFβ for breast cancer therapy, since Smad2 appears only to be required for TGFβ responses that might promote tumorigenesis (migration and invasion) and not for potentially tumor suppressive responses (growth inhibition and apoptosis). This evidence concerns the gene TGFB1 and breast carcinoma.