The same investigators also showed that, unlike CCR2-/- mice, CCL2-/- mice are not protected from FITC-induced lung fibrosis, as they are still able to recruit fibrocytes to injured lung tissue, suggesting that CCR2 ligands may play a role in human disease because the recruitment of human fibrocyte precursors (CD14 + CD16- monocytes) into inflamed tissue is dependent on CCR2 [33]. The gene discussed is CCR2; the disease is pulmonary fibrosis.