The mechanisms that regulate the complex pathways involved in airway inflammation in asthma can be broadly dichotomized into two different endotypes: type 2 (T2) endotype, under the coordination of Th2 lymphocytes and ILC2, which produce IL-5, IL-4 and IL-13, and non-type 2 (non-T2) endotype in which eosinophilia is absent [3]. The gene discussed is IL4; the disease is asthma.