In addition, the role of IL-17A in asthma pathogenesis is incompletely understood, with variable reports of association with disease parameters.4, 64, 65 Indeed, although numbers of both IFN-γ+ and IL-17A+ TH cells were increased in lungs of patients with severe asthma and a mouse model of severe asthma, only knockout of IFN-γ, but not the IL-17A receptor, was sufficient to improve lung function in these mice.9 The gene discussed is IL17RA; the disease is asthma.