Both genes were upregulated in IPF lung tissues compared to healthy controls [54,108], and SMAD-dependent luciferase activity assays suggested that the latent forms of TGFβ2 and TGFβ3 initiate profibrotic signaling without activation, unlike TGFβ1 [54]. The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.