The use of ASC, in turn, was demonstrated to inhibit epithelial‐to‐mesenchymal transition (EMT) and consequently renal fibrosis.61, 62 Analogously to EndMT, EMT is a fibrotic process induced by TGF‐β and mediated by key transcription factors such as Smad2/3, Snail and Twist.63, 64 The effects demonstrated with the use of ASC in EMT are an important indicator that these cells would also play a role in EndMT; thus, our findings on endothelial cells are also in agreement with the findings described for epithelial cells. The gene discussed is SMAD2; the disease is renal fibrosis.