In AECs, FAK1 is activated by Gal‐1 and mediates the transdifferentiation of myofibroblasts, resulting in pulmonary fibrosis.[265] Gal‐3, which is generally expressed in endothelial cells, fibroblasts, and resident alveolar macrophages, is the most studied galectin in pulmonary fibrosis caused by SARS‐CoV‐2. This evidence concerns the gene LGALS3 and pulmonary fibrosis.