We also confirm and extend the findings of senescent alveolar epithelial cell and fibroblast interaction by characterizing the aberrant and SADD phenotype of bleomycin-treated primary AECs (Figure 3E) and by demonstrating a shift toward ECM catabolism and inflammation that is consistent with fibroblast senescence and IPF phenotypes, despite not observing increases in Cdkn1a or Cdkn2a in NHLFs themselves following senescent AEC conditioned medium transfer. This evidence concerns the gene CDKN1A and idiopathic pulmonary fibrosis.