In brief, existing evidence shows that C/EBPα upregulation inhibits fibroblast activation by restraining α-SMA, FN, Col1a1, and CTGF expressions and suppresses the ECM production in alveolar epithelial cells through inhibiting its EMT and promoting the activity of antiprotease alveolar epithelial cells, indicating that targeting C/EBPα may be an effective strategy to treat pulmonary fibrosis. Here, CCN2 is linked to pulmonary fibrosis.