Cystic fibrosis (CF) is characterized by persistent neutrophilic lung inflammation that begins early in life and leads to an inexorable progressive loss of lung function over time, causing significant morbidity and mortality. Studies to date support the hypothesis that higher levels of lung inflammation lead to worsening lung dysfunction. However, measuring the extent and severity of lung inflammation in the CF lung is difficult as few lung-specific biomarkers of inflammation can quantify the regional and whole-lung inflammatory burden accurately and reproducibly. PET with 18F-fluorodeoxyglucose ( 18F-FDG) has shown promise in measuring lung inflammation in both acute and chronic lung diseases. Several studies have now shown that 18F-FDG uptake may be a useful measure of lung inflammation in CF. The whole-lung rate of 18F-FDG uptake in stable CF, quantified by the Patlak graphical analysis, appears to correlate with more rapidly declining lung function. Acute exacerbation, on the contrary, leads to focally increased 18F-FDG uptake, which decreases with antibiotic treatment. These small studies are the first attempts to characterize the patterns of 18F-FDG uptake in CF and suggest a potential role for 18F-FDG as a treatment modifiable biomarker of lung inflammation in CF.