In idiopathic pulmonary fibrosis, TGF-β1 markedly elevates Adam19 mRNA, whereas silencing Adam19 curtails collagen deposition and lung scarring.31 A parallel mechanism operates in the kidney: TGF-β up-regulates Adam19, an effect attenuated by the Smad2/3 inhibitor SB525334, and high Adam19 expression accompanies profibrotic, pro-inflammatory renal decline.32,33 Moreover, Gao et al.34 revealed that Adam19 was closely related to the TGF-β1 pathway and cardiac fibrosis. The gene discussed is SMAD2; the disease is pulmonary fibrosis.