In asthma (particularly T2-high severe asthma), eosinophils are actively recruited to airway tissues in response to chemokines upregulated by IL-4 and IL-13 such as eotaxin-1 (CCL11), eotaxin-2 (CCL24), and eotaxin-3 (CCL26), which binds to CCR3 receptors on eosinophils [37]. This evidence concerns the gene IL4 and asthma.