With airway hyper-responsiveness being the physiological hallmark of asthma, it is also characterized by chronic inflammation of the respiratory tract, allergen-specific IgE production, infiltration of eosinophils, the recruitment of T cells into the airways, and alterations in the fine balance between type 1 helper T lymphocytes (Th1) and type 2 helper T lymphocytes (Th2) responses towards Th2 bias [2]. This evidence concerns the gene IGHE and asthma.