SMAD3 and idiopathic pulmonary fibrosis: In addition, following treatment of PCLuS with 10 μM GB0139 for 4 days, proteomic analysis confirmed that several signaling pathways were downregulated and these included proteins associated with canonical TGF-β1 Smad signaling (transcriptional activity of Smad2/Smad3:Smad4) in each of the IPF patient–derived PCLuS indicating that galectin-3 inhibition reduces downstream signaling from the TGFβRI (Table S2).