We acknowledge that while the presence of COPD-related inflammatory signaling within some of our tissue specimens may have influenced the migration of eosinophils it was unlikely to influence the extracellular pattern of deposition of MBP, nor the interpretation of MBPs rather restricted diffusion and ability to deposit within the airway wall, and hence influence directly myocyte function in vivo. This evidence concerns the gene MBP and chronic obstructive pulmonary disease.