IL-4 activates B cells to differentiate into plasma cells that generate immunoglobulin E (IgE) required for mast cell responses to allergens; IL-5 promotes eosinophil differentiation and survival; IL-13, IL-4, and other inflammatory mediators promote goblet cell overexpression, increased mucus secretion, as well as airway hyperresponsiveness, then contributing to the hallmarks of asthma pathophysiology (7, 11–13). This evidence concerns the gene IL4 and asthma.