Interestingly, immune cell-fibroblast interactions through mediators such as CCL18, CCL2, CX3CL1, CXCL1, IL-6 and IL-8 also contribute to inflammatory mechanisms that may add to tissue remodeling in IPF and need further investigation to ascertain the role of inflammatory mechanisms in IPF therapeutics. This evidence concerns the gene CXCL1 and idiopathic pulmonary fibrosis.