Although the Cox-2 gene is transcriptionally-controlled (e. g. via NF-κB in response to IL-1β [33] or CSE [26]), and mechanisms such as protein turnover contribute to COX-2 expression [34], the level of COX-2 protein is determined in large part by changes in the half-life of the mRNA Thus, there is often a poor correlation between Cox-2 mRNA and protein levels because Cox-2 mRNA is rapidly degraded [4], raising the possibility that mRNA degradation could be why there is discord between mRNA and protein levels in COPD lung fibroblasts. This evidence concerns the gene PTGS2 and chronic obstructive pulmonary disease.