Chronic obstructive pulmonary disease (COPD) is a lethal disease that is predicted to become the third leading cause of death globally within 3 years. 1 Recent research has highlighted the heterogeneity of the pathologic characteristics of COPD, indicating that disease mechanisms are complex. Inflammatory pathways implicating neutrophils have been emphasized, 2 but attention has recently focused on the persistent blood and airway eosinophilia that is found in up to 40% of patients with COPD, even in the absence of a history of asthma; such patients have a higher risk of exacerbations than patients without eosinophilia. 3,4 Guidelines have generally recommended a “one size . . .