Many similarities between the MHV68 model system in IFNγ unresponsive mice and human IPF have been described, including infection and apoptosis of alveolar epithelial cells, type II pneumocyte hyperplasia, epithelial to mesenchymal transition, and M2 macrophage differentiation in the lung [12–14]. Here, IFNG is linked to idiopathic pulmonary fibrosis.