The following factors have been reported to be linked to a poor or slow response to omalizumab treatment: type IIb autoimmunity, characterized by positive results in autologous serum skin tests; the presence of IgG autoantibodies against IgE, FcεRIα, and thyroid antigens; elevated basophil histamine release; and increased expression of basophil FcεRI.11 This evidence concerns the gene FCER1A and Autoimmunity.