Anti–IL-5 therapy represents one of the few attempts to translate findings in mice to humans—and it has failed. IL-5−/− mice were protected both from acute allergic inflammation, airway hyperresponsiveness (10), and chronic airway remodeling (11). However, clinical trials using IL-5 antagonists in both mild acute asthma (12) and chronic severe asthma (13) failed to provide a clinical benefit. These findings put both eosinophil lovers and animal researchers on the defensive. (Note: human researchers claim the Th2 hypothesis as theirs, but they are more than happy to blame the failure of the trials on the mice.) The eosinophil community has been quick to point out that the number of patients in these studies was few, and that approximately 50% of tissue eosinophils persisted. A recent study using eosinophil lineage ablation, achieved by deleting a GATA −1 promoter site, showed that eosinophils are only important in aspects of chronic remodeling (collagen deposition, smooth muscle mass) (14). Given these findings, perhaps anti–IL-5 therapy could be effective in preventing but not reversing established asthma. Although this interpretation may not be clinically useful, it is consistent with the animal findings.