Next, if aggressive intervention does meaningfully delay decline of FEV1, as this report suggests, we must determine which interventions are most effective in which type of patients with CF. There are significant data in the current literature, based on our understanding of the pathogenesis of CF lung disease, to support that inflammation and infection progress in the absence of an acute exacerbation or significant clinical deterioration,1–2 even in clinically stable infants.3–5 The pathophysiologic premise is borne out in a few clinical studies of early or aggressive therapy, including the tobramycin solution for inhalation (TOBI; Chiron Biopharmaceuticals; Emeryville, CA) trial,6the dornase alfa early intervention trial,7the antibiotic prophylaxis in cystic fibrosis study,8and the ibuprofen trial.9 Further, a growing body of clinical data suggest that early anti-inflammatory therapy9–10 and early antimicrobial therapy11reduce the frequency and duration of chronic infection with possible delays in the progression of CF lung disease. Yet, according to recently published data by Oermann and colleagues,12“despite a compelling rationale and considerable interest in the use of anti-inflammatory drugs to slow pulmonary deterioration in CF patients, little is known regarding the prevalence of their use and nothing is known regarding the prescribing patterns of these drugs among CF care providers.” This statement also may be applicable to antibiotic therapies as well. Study data support the use of aggressive antibiotic intervention to prevent13or delay14–15 the acquisition of P aeruginosa in patients with CF to preserve lung function. Long-term intermittent inhaled antibiotic prophylaxis16 has been shown to improve and modify the rate of lung function decline observed in patients with CF (when compared to patients with CF not receiving ongoing prophylaxis). However, it remains unclear which single approach—or combination of strategies—yield the best outcome.