The understanding of EGPA continues to advance, but many gaps in knowledge remain. The nomenclature remains a source of conceptual variance in terms of demonstrated presence or not of vessel inflammation or ANCAs in the diagnosis of EGPA. Distinguishing EGPA from hypereosinophilic syndromes can be problematic, and an understanding of the mechanistic relation between the vasculitis and the eosinophilic proliferation is profoundly lacking. Some evidence suggests distinct disease phenotypes, but this concept has not yet been translated to phenotype-adapted therapy.