Although the traditional view attributes asthma to Th2 cell-mediated inflammation—where Th2 cells induce eosinophil infiltration and IgE production by secreting IL-4, IL-5, and IL-13 (33, 34)—studies have shown that some patients may exhibit non-T2-type inflammation, such as immune responses mediated by Th1 and Th17 cells [31a]. This evidence concerns the gene IL4 and asthma.