Given that it is not clear to what extent the adaptive immune system is involved (aspecific activation of polyclonal T cells by superantigens, non–IgE-mediated antifungal response, local production of IgE in the absence of systemic allergy) in the complex inflammation of CRS [6, 7], it seems logical that the innate immune reactions are so carefully considered in the pathogenesis of CRS. Here, IGHE is linked to congenital rubella syndrome.