JUN and pulmonary fibrosis: Here, we compared our genetic model to the frequently used bleomycin-induced model of lung fibrosis and found that the fibrotic response in the chemical-injury model was similar to our genetic lung-fibrosis model, i.e., similar distinct cell lineages [CD45+ leukocytes, EpCAM+ epithelial cells, CD31+ blood vessel endothelial cells and lineage negative fibroblasts (CD45-EpCAM-CD31-)] clustered together by X-shift clustering (Fig. 6a), and both resulted in activation of phospho JUN (Supplementary Fig. 6a).