Thus, in contrast to the Type 2 (T2 or eosinophilic) type of asthma which was mediated by IL-4, IL-5, and IL-13, the profile of the inflammatory mediators with high levels of IL-6, CXCL8, and IFNγ after TLR stimulation mirrored that of the non-T2 endotype of asthma [57–59]. The gene discussed is IL13; the disease is asthma.