At this moment of tremendous excitement, it is easy to lose sight of the rest of the development pipeline.2 The drugs that it describes include inhaled tobramycin (TOBI) and aztreonam (Cayston), azithromycin, dornase alfa (Pulmozyme), hypertonic saline, pancreatic enzyme products (including Ultresa, Zenpep, Pancreaze, Viokace, Pertzye, and Creon),5 and fat-soluble vitamin preparations, all of which have already had a tremendous impact on the quantity and quality of life of people with CF. Beyond these available medications, new therapies are under evaluation that will likely improve and extend the lives of individuals with CF, regardless of the impact of CFTR-targeted compounds. People who already have CF lung disease, and those for whom effective CFTR genotype-specific compounds are not yet available, need better antibiotic, antiinflammatory, mucus-altering, and nutritional therapies, among others; some may need transplantation. Recent advances in cell- and gene-based techniques have also revived interest in genetically repairing (rather than chemically restoring) CFTR function. In this review, we focus on these promising therapies in development specifically for CF lung disease, with reference to those currently in use. In summarizing what is to come, we hope to show that the excitement generated by Kalydeco promises to be just the beginning of a new era in the field of CF therapeutics.