Both Th2 cells and ILC2 cells contribute to eosinophilic inflammation by upregulating the expression of GATA-3 which can promote the production of Th2 cytokines, upregulate the expression of chemokine receptors such as CCR4, CCR8 and CRTH2, and increase the production of IL-5 to modulate the development of eosinophils, IL-13 leading to goblet cell metaplasia and bronchial hyperreactivity, IL-4 affecting the mature and activation of Th9 cells which can promote the IgE synthesis by B cells. The gene discussed is IGHE; the disease is asthma.