Nevertheless, this view of the IgA response as a pathogenic mechanism in AR acting along with IgE, is contested by several observations: first, SIgAD or delayed serum IgA production in childhood is a well-known risk factor for atopy (97, 98) and patients with sIgAD suffer more frequently from AR compared to the general population (71, 72). The gene discussed is CD79A; the disease is selective IgA deficiency disease.