IL-4 and IL-13 can promote the expression of EOS chemokines, promote EOS adhesion and migration in the airway, increase the amount of EOS in the airway, and then secrete a large amount of granuloprotein, cytokines, and chemokines, leading to the damage of airway endothelial cells and mucous membranes, and eventually trigger asthma [76]. The gene discussed is IL4; the disease is asthma.