The greater effect by GM-CSF and IL-3 than IL-5 on eosinophil adhesion at 1 h and migration over 20 h, respectively, may motivate therapeutic targeting of GM-CSF or IL-3, or their receptors, in addition to or as an alternative to IL-5 or its receptor, in order to inhibit activation of eosinophils and their interactions with matrix in tissues in eosinophilic diseases. This evidence concerns the gene CSF2 and eosinophil disorder.