Xianghong Zhang et al. reported that both Sp1 and SMADs (SMAD2, SMAD3, SMAD4) induced the expression of MET by binding to MET promotor (SMAD binding element, SBE) in renal epithelial cells.24 Recent studies found MET promoter contained a putative binding site for SMADs, and this binding activity was constitutively upregulated in systemic sclerosis fibroblasts as well as in normal fibroblasts treated with exogenous TGF-β1.25 Whether SMADs have the same effect on MET in tumors, especially BCa, no studies have elucidated. Here, TGFB1 is linked to systemic sclerosis.