Studies show that the chemokine CCL1, derived from alveolar macrophages, is aberrantly up-regulated in pulmonary fibrosis; binding of CCL1 to autocrine motility factor receptor (AMFR) on lung fibroblasts activates the AMPKα-FOXO3–Snail axis, driving fibroblast-to-myofibroblast differentiation and Snail-mediated EMT, thereby accelerating fibrosis (30). The gene discussed is AMFR; the disease is pulmonary fibrosis.