Given the complex dual role of TGFβ in breast cancer tumorigenesis, and the desire to generate TGFβ pathway antagonists that might selectively block pro-progression and not tumor suppressor activities of TGFβ, we wished to determine whether the two TGFβ R-Smads contribute differentially to these two classes of activity in the normal and transformed mammary epithelium. Here, TGFB1 is linked to neoplasm.