However, since AATD individuals with normal spirometry (AATDPFTnorm) did not have elevated CRP, and yet exhibit a similar low circulating AAT as AATD-AUG with COPD (Table 1), it seems more likely the elevated CRP is associated with the pathophysiology of the COPD sequelae rather than a response to polymers associated with α1-antitrypsin allele variants. This evidence concerns the gene CRP and chronic obstructive pulmonary disease.