In fact, as is the case of T2-high and T2-low asthma, underlying immunopathophysiological mechanisms (involving cytokines) have been identified and there is even effective medication targeted at these mechanisms (e.g., anti-IgE, anti-IL-5, anti-IL-5 receptor or anti-IL4/IL3 receptor α-chain) [87]. This evidence concerns the gene IL4 and asthma.