Although COPD SAFs displayed no significant difference in fibrotic marker expression compared with nonsmoker or smoker SAFs (Supplemental Fig. S8), pathway analysis of the senescence-enriched COPD SAFs suggested enrichment for pathways associated with fibrosis, IL-6, TGFβ, and Wnt/β-catenin signaling (Fig. 6C). This evidence concerns the gene TGFB1 and chronic obstructive pulmonary disease.