Cell division cycle 42 (Cdc42) acts on the polymerization of actin in AT2 cells, and its deletion causes a sustained increase in mechanical tension in AT2 cells, leading to activation of the TGF-β pathway, driving the comprehensive development of fibrosis from the periphery to center, with low Cdc42 expression in IPF patient samples [35,38]. The gene discussed is TGFB1; the disease is idiopathic pulmonary fibrosis.