SMAD2 and neoplasm: These MDSCs promoted mesenchymal-epithelial transformation (MET) of metastatic tumor cells within the lung metastases by expressing versican, which blocked TGF-β-Smad2 mother against decapentaplegic 2 (Smad2) pathway-mediated EMT, and in turn, promoted the growth of tumor lesions at the metastatic sites (71).