A lot of us in asthma are interested in drug resistance. In my presentation, I mentioned that a variation around the ninth axon of the glucocorticoid receptor gene produces the β-isoform, which is inactive as a receptor. So, individuals with a more prominent β-isoform would be expected to be resistant to corticosteroid therapy. In addition, the gene itself has a large promoter region that extends through the first axon, which regulates activity. Variation in that area, we could hypothesize, may determine how responsive an individual is to corticosteroid therapy, and this may answer, in part, why there is variation in response in both asthma and COPD.