Experimental mouse models of asthma have shown that allergen exposure protocols induce immune-mediated airway inflammation defined by: elevated levels of asthma biomarkers (IgE, the T-helper cell 2 (Th2) cytokines, interleukins (IL)-4, -5 and -13, and eosinophils), induction of airway remodeling (increases in airway smooth muscle, collagen deposition and goblet cell hyperplasia), and BHR that is sustained after the resolution of eosinophilic inflammation [21,22,23]. This evidence concerns the gene IL4 and asthma.