Anti‐neutrophil cytoplasmic antibody (ANCA)‐associated vasculitis (AAV) consisted of granulomatosis with polyangiitis (GPA), eosinophilic granulomatosis with polyangiitis (EGPA) and microscopic polyangiitis (MPA).1 AAV is characterized by pauci‐immune necrotizing small vessel vasculitis which principally involves glomerular endothelial cells (GEnCs) injury, and circulating autoantibodies against myeloperoxidase (MPO) as well as proteinase 3 (PR3).2, 3 MPO‐ANCA was reported to induce GEnC activation directly in AAV.4 The gene discussed is PRTN3; the disease is anti-neutrophil cytoplasmic antibody-associated vasculitis.