This (i) is regulated through the kinase activity of the BMP type I receptor and (ii) requires the direct involvement of SMAD4 in MCF7 human breast cancer cell line, potentially through the suppression of TGF-β signaling, indicating that the previously described crosstalk between BMP and WNT pathways [25,26,27,28,29] can also be extended to breast cancer. This evidence concerns the gene SMAD4 and breast carcinoma.