A key finding was that NFATc3 deficiency significantly attenuated BLM-induced pulmonary fibrosis and inflammation, and the adoptive transfer of NFATc3+/+ macrophages into NFATc3+/- mice restored cellular and pulmonary fibrotic markers in mouse models of BLM-induced pulmonary fibrosis. This evidence concerns the gene NFATC3 and pulmonary fibrosis.