It is possible that the measurements of aSMase activity are more sensitive than EMPs counts to detect COPD; that EMPs abundance is more closely related to certain disease phenotypes that are not linked to GOLD severity; or that a plateau is reached in aSMase-dependent EMPs release which may be proportional to the lung capillary surface area, (lost with increasing COPD severity). This evidence concerns the gene SMPD1 and chronic obstructive pulmonary disease.