Variants in C3 have been associated with asthma [64] and mice deficient in C3 exhibit diminished airway hyper-responsiveness and lung eosinophilia when challenged with allergen [65]; also, NOTCH1 is involved CD8+ T cell-mediated development of airway hyper-responsiveness and inflammation [66], while ITGAL/ITGB2 mediates altered responsiveness of atopic asthmatic airway smooth muscle in rabbits [67]. This evidence concerns the gene NOTCH1 and Increased total eosinophil count.