In mice, inflammatory eosinophils (iEos)—the primary targets of anti-IL-5 biologics in asthma—may be dependent on IL-5 for activity, whereas rEos may not be.16 This would suggest that benralizumab, a high-affinity IL-5 receptor antagonist,17 would deplete both iEos and rEos through NK-mediated killing, whereas mepolizumab, an anti-IL-5 monoclonal antibody,17 may deplete iEos but keep rEos intact. The gene discussed is IL5; the disease is asthma.