Collectively, these data suggest that additional pathways [24] are also likely to contribute to the IPF-like pathologies that develop in this model, which is consistent with our observations that other pro-fibrotic mediators (e.g. LPA) and pathways (e.g. Wnt, PDGF) are up-regulated during the fibrotic phases of the response to bleomycin. This evidence concerns the gene LPA and idiopathic pulmonary fibrosis.