Second, although inhibition of the recruitment of inflammatory cells as well as TGF-β1, CTGF, α-SMA, and PAI-1 expression were observed during fasudil administration, the detailed mechanisms by which fasudil acts to prevent bleomycin-induced pulmonary fibrosis remain to be determined in the context of the pleiotropic effects of fasudil and the complex pathogenesis of pulmonary fibrosis. This evidence concerns the gene TGFB1 and pulmonary fibrosis.