In line with our study, Tomcik et al. [34] reported that TGF-β1 induced S100A4 expression, and enhanced fibroblast activation in systemic sclerosis most likely via the induction of the canonical TGF-β/Smad pathway, indicating that S100A4 and TGF-β/Smad can regulate each other to form a vicious cycle. The gene discussed is S100A4; the disease is systemic sclerosis.