In vivo, the authors demonstrated that the intratracheal administration of Ad.CAV1 attenuated BLM-induced pulmonary fibrosis by suppressing TGF-β1-induced ECM production in pulmonary fibroblasts and modulating TGF-β1-induced SMAD signaling and COL1A1 production via the ERK1 pathway. The gene discussed is TGFB1; the disease is pulmonary fibrosis.