In a rat nephrectomy model, overexpression of Smad7 blocked TGF-β/Smad signaling, and thereby inhibited miR-192 expression and renal fibrosis, suggesting that miR-192 may be an important downstream of the TGF-β/Smad3 signaling pathway [43]. The gene discussed is TGFB1; the disease is renal fibrosis.