In the setting of lung injury, LPA has been shown to contribute to epithelial cell death, increased vascular permeability, and fibroblast migration and persistence via interaction with the LPA1 receptor, and genetic deficiency or pharmacologic inhibition of LPA1 confers protection against bleomycin-induced lung fibrosis in mice [13,18,19]. This evidence concerns the gene LPAR1 and pulmonary fibrosis.