Together, these data reinforce a growing body of evidence describing the role of the metastatic microenvironment in regulating DTC outgrowth44–46 and support a model in which the PDGF-Chi microenvironment supports rapid metastatic outgrowth in aged mice or mice with lung fibrosis by acting to recruit and activate PDGFRα-positive fibroblasts and increase tPA levels, required for proteolytic cleavage of the PDGF-C precursor. This evidence concerns the gene PDGFC and pulmonary fibrosis.