Indeed, the co-occurrence of anti-FcεRI IgG and IgE autoantibodies in late- and non-responders, but not in early ones, credits the co-existence of autoimmune (i.e., type IIb autoimmunity) and autoallergic (i.e., type I autoimmunity) mechanisms as a driver of late/poor response to omalizumab. This evidence concerns the gene IGHE and Autoimmunity.