The most well‐described galectin in relation to mucins is Gal‐3 that can interact with MUC1, MUC4 and MUC16 to alter cell surface polarisation, enhance tumor cell homotypic aggregation and increase growth factor signalling pathways.28, 47 The observation that the Gal‐3 knockout mouse is resistant to bleomycin‐induced lung fibrosis,48 and Gal‐3 is highly expressed in fibrotic tissue, suggested Gal‐3 as a potential therapeutic target in fibrotic lung disease. This evidence concerns the gene LGALS3 and pulmonary fibrosis.