In vivo, many airway inflammatory mediators are increased in asthmatic patients including thymic stromal lymphopoietin (TSLP), eotaxin-1 and granulocyte-monocyte colony-stimulating factor (GM-CSF), which have been shown to drive eosinophilia and TH2-inflammation (interleukin (IL)-4, IL-5, IL-9, IL-13), whereas in neutrophilic asthma, IL-8, IL-6, IL-1, and tumor necrosis factor (TNF)-α have been shown to drive chronic airway inflammation [6]. The gene discussed is IL6; the disease is Increased total eosinophil count.