However, UPR can also participate in pulmonary fibrosis by increasing the expression of profibrotic mediators, such as TGF-β1, platelet-derived growth factor (PDGF), CXCL12, and CCL2 (Zolak and de Andrade, 2012; Wolters et al., 2014). The gene discussed is CCL2; the disease is pulmonary fibrosis.