As Smad3 but not Smad2 is the primary effector of TGF‐β signaling to mediate EMT and fibrosis in the epithelial cells,[36, 37] it is highly possible that Btg2 may orchestrate the downstream TGF‐β/Smad3 signaling to mediate podocyte injury in FSGS. This evidence concerns the gene TGFB1 and focal segmental glomerulosclerosis.