The focused data of Kanazawa et al correlate the higher levels of oxidative products (nitrates and nitrites) found in the induced sputum of asthmatics with lower levels of an antioxidant marker, PNIA, compared with normal control subjects. They further demonstrate the reversal of these pertubations and parallel improvement of airways function (FEV1) in response to inhaled corticosteroids (BDP). What can this mean? Clearly, it provides even more support for the first-line use of inhaled corticosteroids in the treatment of asthma. The obvious reasoning is that asthma is, in part, characterized by airway inflammation, steroids are anti-inflammatory, markers of inflammation revert toward normal with BDP use, and airways function improves. But what are the implications of this substantial yet only partial reversal toward normal? Does that mean that a higher BDP dose is likely to provide even more functional improvement? Or, alternatively, is the reversal in response to inhaled steroids limited by factors unassociated with the drug action, per se? Is clinical response limited by drug distribution, complexity of molecular and cellular mechanism causing disease, or complications of the disease (ie, bacterial infection) not affected by BDP? Also, one might consider a situation when biochemical markers remain unchanged and abnormal in response to a standard dosage of inhaled corticosteroids. Does that mean that a higher dose is required? Or does this imply that alternative therapy must be considered possibly because inflammation is already maximally improved and that other mechanisms yielding an asthmatic phenotype are operative or remodeling has taken place? Or is the diagnosis wrong?