At present, the pathogenesis is believed to be mainly ANCA-mediated vascular wall damage and eosinophil infiltration-mediated damage.[3] Studies have shown that ANCA can activate neutrophils to generate reactive oxygen species and release lysosomal proteolytic enzymes, which can affect the function of vascular endothelial cells and increase vascular permeability.[4] Clinically, 30% to 50% of patients with EGPA are ANCA positive, with MPO-ANCA accounting for 71.4% to 100% of ANCA-positive cases. The gene discussed is MPO; the disease is eosinophilic granulomatosis with polyangiitis.