Here, we have uncovered a causal link between the disruption of TGFβ signaling in high grade breast cancer and the constitutive activation of BST2. Our data suggest that aberrant BST2 overexpression promotes the consequences of obliterated TGFβ-mediated tumor suppressive effects in breast cancer, and subsequent loss of differentiation programs. This evidence concerns the gene TGFB1 and breast carcinoma.