Apoa1-deficient mice that were sensitized and challenged with ovalbumin developed augmented neutrophilic airway inflammation that was primarily mediated by the increased production of granulocyte colony stimulating factor (G-CSF) by alveolar macrophages (AMφs) and PVECs, as well as by the increased expression of IL-17A, TNF-α, CXCL5, and VCAM-1 (Dai et al., 2012). The gene discussed is CSF3; the disease is inflammatory response.