Although mast cell activation via IgE-mediated pathways is postulated to have a pivotal role in anaphylaxis, there has been steady progress in understanding that other pathways, effector cells and mediators potentially contribute to symptoms (1), with evidence for a potential role involving complement, basophils, neutrophils, monocytes/macrophages, platelets, and mediators, such as platelet-activating factor (PAF), cysteinyl leukotrienes (CysLTs), tryptase, and cytokines/chemokines (1, 5–9). This evidence concerns the gene IGHE and anaphylaxis.