Although lung injury promotes the release of CCL2 by several different lung cell types, including airway epithelial cells, and serves as a chemoattractant for CCR2 pro-fibrotic macrophages [47, 48], CCL2 neutralizing antibodies did not alter disease progression or mitigate lung function decline in patients with idiopathic pulmonary fibrosis, but instead was associated with an increase in endogenous CCL2 expression and other adverse compensatory changes [49]. The gene discussed is CCR2; the disease is idiopathic pulmonary fibrosis.