It is generally believed that the Smad-dependent pathway is involved in TGF-β tumor suppressive functions at an early stage of cancer development, whereas activation of Smad-independent pathways is coupled with the loss of tumor-suppressor function of TGF-β, which is important for its pro-oncogenic effects.30 TGF-β enhances the protein level of KLF17 in multiple cancer cell lines. This evidence concerns the gene TGFB1 and neoplasm.