To examine the mechanisms of omalizumab’s effects, we examined the association between the clinical markers of eosinophilic airway inflammation, such as CCL4, CD69, and IL-13, an inducer of iNOS [23] and PP2A (which regulates corticosteroid sensitivity via nuclear translocation of the glucocorticoid receptor), in BEAS-2B airway epithelial cells. This evidence concerns the gene CD69 and inflammatory response.