Identifying the most appropriate pathogenic pathways—by inhibiting IL-5 in patients with eosinophilic phenotypes, IL-4/IL-13 in severe T helper 2 (Th2)-type asthma, or IgE inhibitors for allergic asthma—has led to substantial progress in disease control, with broader possibilities for blocking the inflammatory process. The gene discussed is IL4; the disease is asthma.