Reasons underlying this might be the difficulty in the identification of the self-antigens that trigger autoimmunity, the inability of regulatory T cells to suppress cytokine production under inflammatory conditions, the different immune players participating in allergies compared to MS (e.g., IgE antibodies, Th2 responses), and also the route, dosage, and timing used for ASI treatments [128]. This evidence concerns the gene IGHE and allergic disease.