Immunohistological analysis also showed that CCL3 and S1PR2 were co-expressed on the airway ECs in the experimental asthma mouse model, and the expression level of CCL3 was attenuated by JTE013, although the expression level of S1PR2 was not attenuated by JTE013 because JTE013 only inhibits S1P binding to S1PR2 (Fig. 3a). The gene discussed is S1PR2; the disease is asthma.