Due to the local upregulation of CCL22 in inflamed and/or fibrotic lung tissue, for instance in patients diagnosed for asthma or idiopathic pulmonary fibrosis (149, 150), its proven capacity to chemoattract ILC2s (26, 132) and the presence of the corresponding chemokine receptor CCR4 on the vast majority of circulating ILC2s (109), the CCL22/CCR4 axis emerged as an attractive target for controlling the additional pulmonary recruitment of peripheral ILC2s in the course of inflammatory lung diseases. This evidence concerns the gene CCR4 and asthma.