Smad3 in particular was implicated in driving the myofibroblast phenotype in healthy parenchymal HLMFs [21], and while we found that both Smad2 and Smad3 mRNA were increased in IPF-derived HLMFs, Smad3 mRNA was significantly higher than Smad2 in both NFC and IPF-derived cells. The gene discussed is SMAD2; the disease is idiopathic pulmonary fibrosis.