The major importance of IL-5 has been demonstrated by several experiments where its deletion or overexpression in mice led to eosinophil depletion or excessive synthesis, respectively, and by clinical trials in severe asthma patients displaying a profound eosinophil depletion when treated with IL-5 antagonists, leading to a dramatic control of their symptoms and of the need for oral corticoids [11,12,13]. The gene discussed is IL5; the disease is asthma.