As Th17 cells show more functional plasticity and instability than Th2 cells, we propose a hypothesis that the influx of the initial polarization of Th17 cells into the lung is not stably committed at the challenge phase of allergic asthma and subsequently converts into more pathogenic IL-17-producing Th2 cells that sustain persistent mixed eosinophilic and neutrophilic inflammation during the chronic stage of asthma. The gene discussed is IL17A; the disease is allergic asthma.