There was a statistically significant direct correlation in blood of IPF non-smokers among CCL2 levels and percent prevalence of circulating fibrocytes providing external validation to the relevant work of Ekert et al. In IPF, we postulate that in a higher powered study where current smokers with IPF may have lower levels of circulating fibrocytes, CCL2 may, in part, mediate this effect based on the significant reduction in CCL2 levels observed in the current work in IPF smokers versus their non-smoker counterparts. This evidence concerns the gene CCL2 and idiopathic pulmonary fibrosis.