Our findings showed that IgE-hFcεRI-dependent upregulation of co-stimulatory CD80, CD86, and CD40 on hFcεRI eosinophils would be consonant with a recent study of 32 allergic asthma subjects who had clinically beneficial responses over 16 weeks of treatment with the anti-IgE mAb, omalizumab [35]. The gene discussed is CD86; the disease is allergic asthma.