Secondly, the finding that ILC2s can induce eosinophil recruitment, mucus hyperproduction, and airway hyperresponsiveness in the absence of T and B cells in mice warrants further investigation of the relative contribution of ILC2s in comparison with the Th2-IgE-mast cell pathway to the development of shortness of breath, the most relevant clinical symptom in human asthma. The gene discussed is IGHE; the disease is asthma.