Until recently, IgE-mediated MC activation were thought to contribute to atopic dermatitis and allergic contact dermatitis, but it is now realized that MRGPRB2 plays an important role in these responses through its activation by agonists generated from nerve endings (substance P) and keratinocytes (proadrenomedullin N-terminal peptides), respectively (8, 19). Here, IGHE is linked to atopic eczema.