Clinical therapies, such as anti-interleukin (anti-IL)-4/13, anti-IL-5, and D prostanoid receptor 2 (DP2) antagonism, that lead to depletion or prevention of migration of eosinophils, can reduce exacerbation frequency and severity in asthma.[5], [6] It has been suggested that type-2 cytokines play critical roles in the pathogenesis of EA, particularly IL-5 which is a key mediator acting at many levels of eosinophil biology. The gene discussed is IL5; the disease is asthma.