The IgE-dependent inflammatory phenomena have been studied in depth and are clearly recognized in atopic subjects, and the anti-IgE blocking effect of omalizumab has been clearly shown. Additional benefits can be provided by the findings of Kalesnikoff et al,3 who observed that by binding to its high-affinity receptor, FcεRI, IgE was able to induce intracellular signaling pathways, resulting in the production of cytokines and the enhancement of mast-cell survival on its own, without cross-linking by allergens. In addition, IgE can directly bind and activate receptors present on eosinophils, neutrophils, and monocytes. As a result, the rationale for the use of omalizumab in diseases other than allergy is based on its blocking effect on IgE, which inhibits part of the T helper cell type 2 immune response, thus, reducing recruitment and activation of effector cells of the inflammatory process, including eosinophils. Because IgE effector cells (ie, mast cells and basophils) are a source of proinflammatory molecules, anti-IgE therapy may have antiinflammatory properties that reduce circulating and tissue eosinophils4; indeed, this role has been suggested in other diseases, such as eosinophil-associated GI disorders.5 More recently, Noga et al4 demonstrated an increase in eosinophil apoptosis and a decrease in granulocyte-macrophage colony-stimulating factor. All this information can help to explain the benefits of omalizumab in CEP.