Several studies have shown the ES could be a target organ attacked by the allergic reaction (5), viral or bacterial infection (9–11), autoimmunity (13–15), otitis media-induced inflammatory products and toxins (44), circulating immune complexes (45), genetic predisposition to altered NF-κB-mediated inflammatory responses (21) and distinct and altered cytokine profiles (16), resulting in the damage of the epithelial layers surrounding the ES space and the dysfunction of ES. The gene discussed is NFKB1; the disease is bacterial infectious disease.