SMAD4 and neoplasm: The absence of TAp73 and, as a consequence, loss of expression of Smad4 and biglycan led to activation of TGF-β signaling through Smad independent pathway(s), i.e., ERK1/2, favoring oncogenic TGF-β effects and epithelial-mesenchymal transition (EMT) in the tumor cells of TAp73−/− mice.