Besides inducing chemotaxis toward eotaxin, CCR3 was shown to enhance eosinophil viability49 and to be transcriptionally upregulated in allergic asthma.67 Eosinophils bind to endothelial cells mainly via VLA‐4–VCAM interaction68 which—along with CCR3 activation—might be a critical regulator of eosinophil extravasation. This evidence concerns the gene CCR3 and allergic asthma.