Gal‐3 not only activates the inflammatory response and cytokine storm in the lungs but also triggers TGF‐β signaling and leads to EMT, ECM accumulation, and epithelial cell apoptosis.[266, 267] In addition, Gal‐3 can also lead to pulmonary fibrosis through binding to Toll‐like receptor 4 (TLR4).[268] TLRs function mainly in the recognition of virus particles and activation of the innate immune system. This evidence concerns the gene LGALS3 and pulmonary fibrosis.