In addition, it is also noticed that SMAD7 overexpression failed to completely block cancer cell TGFβ responses as revealed by SBE activity, osteoclast differentiation and PTHLH induction (Fig. 5d–f), implying a SMAD7-independent mechanism for the oncogenic role of miR-182 and the TGFβ response of cancer cells. This evidence concerns the gene SMAD7 and cancer.