Similarly to what we found in fibroblasts from diseased aged mouse lungs, UMAP — along with gene expression analysis — revealed increased expression of genes associated with fibroblast activation, including CTHRC1, POSTN, COL1A1, and COL3A1, in a pathogenic fibroblast population in IPF lungs, as previously demonstrated (7) (Figure 3, A and B). Here, CTHRC1 is linked to idiopathic pulmonary fibrosis.