Cystic fibrosis (CF) is the most common inherited disease in the Western world, affecting more than 30 000 individuals in the United States and (SO 000 individuals world�wide. Respiratory failure continues to account for more than 80% of the deaths from this disease. However, ad�vances in treatment have increased the median predicted survival time from I(S years in the 1970s to more than 37 years today. Adults now represent more than 40% of the total CF population (1). As the lifespan of these patients in�creases, so does the complexity of treat�ing their disease. The overriding em�phasis in the clinical care of patients with CF is control of chronic airway in�fections and inflammation and mainte�nance of lung function for as long as possible. More sophisticated measures of disease progression and therapeutic response are in great demand to guide the clinical care of patients with CF, especially those who are very young and those with severe lung destruction, in whom physiologic assessment may be particularly challenging. Multiple thera�pies are being considered. These in�clude administration of antimicrobial and antiinflammatory agents, as well as use of modulators of airway surface liq�uid and the CF transmembrane conduc�tance regulator (or CFTR) gene. There is a critical need for the development of end points that can be used when con�ducting interventional trials of such agents. Ideally, such end points will be sufficiently sensitive to enable drugs to be tested with relatively small sample sizes (2-4).