In individuals with respiratory allergies, the overexpression of the high‐affinity IgE receptor, FcεRI, and their cross‐linking by the culprit allergens has been shown to disrupt virus‐induced IFN‐α responses,10, 24 providing an explanation of why patients with allergic asthma may experience more severe respiratory virus infections. The gene discussed is IFNA1; the disease is allergic asthma.