To elucidate the mechanisms of fasudil-induced inhibition of the pulmonary fibrosis model, the number of inflammatory cells in bronchoalveolar lavage fluid (BALF) as well as TGF-β1, CTGF, alpha-smooth muscle actin (α-SMA), and plasminogen activator inhibitor-1 (PAI-1) mRNA and protein levels in the lungs were examined. The gene discussed is CCN2; the disease is pulmonary fibrosis.