Furthermore, Chi3l1 may promote the progression of IPF and interstitial transformation of alveolar epithelial cells through the TGF-β1/Smad3 signaling pathway, and the Chi3l1–CRTH2 pathway functions in regulating monocyte/macrophage responses in patients with IPF (Figure 2) [33,34]. The gene discussed is SMAD3; the disease is idiopathic pulmonary fibrosis.