Interfering with signals driving the recruitment and/or alternative activation of macrophages in mice lacking CCR2 or by treatment with mAB against CSF-1R or CTGF attenuated radiation-induced lung fibrosis in mice [69,180,269,270], corroborating the pathologic role of alternatively activated macrophages in the development and progression of RILF or radiation-induced renal fibrosis, respectively [270,271]. This evidence concerns the gene CCR2 and pulmonary fibrosis.