Commonly used laboratory markers, such as blood eosinophil count, serum immunoglobulin E (IgE), erythrocyte sedimentation rate (ESR), or C-reactive protein (CRP), do not reliably discriminate active disease in EGPA from non-EGPA disease or damage, and are unpredictably influenced by glucocorticoids and other immunosuppressive therapies[2]. This evidence concerns the gene IGHE and eosinophilic granulomatosis with polyangiitis.