In contrast, although BLM‐induced PF does not perfectly resemble the pathology and chronicity of human PF, BLM remains a well‐established and useful model for studying PF.35, 36 In vivo IM‐1918 administration significantly decreased CTGF, fibronectin, α‐SMA and collagen accumulation in a BLM‐induced lung fibrosis animal model, suggesting that IM‐1918 is a highly efficacious anti‐fibrotic agent with potential for further clinical application. This evidence concerns the gene ACTA1 and pulmonary fibrosis.