Apart from a repressed β-catenin-dependent Wnt canonical pathway that was linked to impaired lung repair in COPD, an enhanced β-catenin-independent noncanonical Wnt signaling was also observed in the lungs from COPD patients and in pulmonary fibroblasts exposed to COPD-related stimuli, such as TGF-β, CS, and cellular senescence. The gene discussed is CS; the disease is chronic obstructive pulmonary disease.