Classical allergic asthma, associated with a type 2 immunity response, is predominantly driven by the activation of T helper 2 (Th2) lymphocytes, which orchestrate a cascade of pro-inflammatory events characteristic of the type 2 immunity-high phenotype [4], as characterized by excessive production of immunoglobulin E (IgE) and type 2 cytokines such as IL-4, IL-5 and IL-13, as well as eotaxin-1, a selective eosinophil chemoattractant CCL11 chemokine, all of which play crucial roles in asthma [2,3,4,5]. This evidence concerns the gene IGHE and asthma.