While transient Fgf10 expression by ASMCs is critical for proper airway epithelial regeneration in response to injury, sustained FGF10 secretion by the ASMC niche, in response to chronic ILK/HIPPO inactivation, results in pathological changes in airway architecture resembling the abnormalities seen in COPD. The gene discussed is ILK; the disease is chronic obstructive pulmonary disease.