However, the rigidity of lung tissue in IPF patients sharply increases due to the accumulation of myofibroblasts with an elevated modulus of 30–50 kPa.[216] Furthermore, mechanosensitive α‐integrin on myofibroblasts plays a critical role in promoting fibrosis via the activation of TGF‐β.[218, 219] A stiff matrix promotes pulmonary fibrosis by activating β1 integrin and focal adhesion kinase (FAK) in fibroblasts.[220, 221] This evidence suggests that the integrin signaling pathway functions in integrating several signals to regulate myofibroblast transformation.[222]. This evidence concerns the gene TGFB1 and pulmonary fibrosis.