Having observed clearly augmented pro-inflammatory mediator responses to EGF-stimulation of PBECs from patients with Mod/Sev asthma, their relative roles were analysed using neutralising monoclonal antibodies (mAb) against GM-CSF and TNF-α and IL-6R (for neutrophil survival) and the selective antagonist for the CXCR2 receptor, SB-225002 (for neutrophil chemotaxis) at concentrations validated previously [14]. The gene discussed is EGF; the disease is asthma.