Interestingly, blockade of Smad3 signaling with a Smad3 inhibitor SIS3 is also capable of inhibiting Btg2 expression and Btg2‐mediated podocyte EMT, revealing a TGF‐β/Smad3‐Btg2 circuit mechanism in Btg2‐mediated podocyte injury in FSGS. The gene discussed is BTG2; the disease is focal segmental glomerulosclerosis.