However, in HDM-induced asthma, transfer of IL-4/IL-13−/− B cells into μMT mice reduced airway hyperresponsiveness but had no effect on the Th2 response or airway inflammation—suggesting that IL-4 responsiveness, rather than IL-4 production by B cells, drives Th2 responses and airway inflammation (21). The gene discussed is IL4; the disease is airway hyperresponsiveness.