Overall, and especially given the relatively small number of individuals per group, the results quite strongly suggest that smoking itself generally stimulates anti-inflammatory HDAC2 expression, but is either modified by the COPD process or is exposing a group of individuals which responds differently to cigarette smoke without an anti-inflammatory HDAC2 response and is therefore vulnerable as a result to developing airway remodelling and fixed obstruction. The gene discussed is HDAC2; the disease is chronic obstructive pulmonary disease.