In addition, in mouse models of pulmonary fibrosis, the lack of NK cell recruitment resulted in the absence of IFN-γ in the lung and enhanced fibrosis; exogenous IFN-γ treatment was therapeutic [32], [33], demonstrating the importance of NK cell-derived IFN-γ in regulating pulmonary fibrosis. The gene discussed is IFNG; the disease is pulmonary fibrosis.