Together, these findings may be of particular importance in the highly oxidative milieu of the asthma or COPD-diseased lung, whereby the creation of redox deficient receptors, plausibly through over-oxidation of β2AR, could facilitate functional decreases in downstream CREB-mediated β2AR expression, an effect that could also in part explain tachyphylaxis to β2-agonists. Here, CREB1 is linked to chronic obstructive pulmonary disease.