After allergens exposure, epithelial cells polarize macrophages, DC cells, T cells, etc. (Frati et al., 2018; Lejeune et al., 2020), releasing not only IL-4, IL-5, IL-13 and other cytokines but also pro-inflammatory cytokines such as IL-25, IL-33 and thymic stromal lymphopoietin (TSLP) activating ILC2 rather than IFN-γ and TNF-β produced by Th1 cells (Lejeune et al., 2020), which causes Th0 cells polarized into Th2 cells in asthma-specific cytokine environments, resulting in a balanced skewed Th2 cellular immune response. The gene discussed is IL33; the disease is asthma.