Further studies into the significance of the co-localization of CXCL14/CXCR4/ACTA2 within the IPF lung needs to be performed, however, we speculate that it may be possible to slow or inhibit fibroblast migration and activation by pharmacological intervention directed at the CXCR4/CXCL14 complex. This evidence concerns the gene ACTA2 and idiopathic pulmonary fibrosis.