This investigation was based on our previous work, where we found that EA regulates the expression of IgE and Th1/Th2 cytokines involved in DNP-KLH immunized mice [11, 12], and some of the studies and clinical experiences have shown that EA reduces the inflammatory response during allergy pathogenesis in an OVA-sensitized model and rheumatoid arthritis [2, 3, 38]. The gene discussed is IGHE; the disease is allergic disease.