Evidence suggests that the potential role of IL-13 in asthma may come from its aptitude to directly interact with airway resident cells, such as epithelial cells or airway smooth muscle (ASM) cells, as shown by the ability of IL-13 to stimulate a set of different pro-asthmatic genes including inflammatory cytokines such as thymus and activation-regulated chemokine (TARC), eotaxin, monocyte chemotactic protein-1 (MCP-1) as well as growth factors such as vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) [6-10]. This evidence concerns the gene CCL2 and asthma.