The molecular pathogenesis of PNH is the mutation of phosphatidylinositol glycan-class A (PIG-A) gene on the X chromosome of hematopoietic stem cells, which leads to the disorder of glycophosphatidylinositol (GPI) synthesis [2], resulting in the deficiency of glycosylphosphatidylinositol anchor protein (GPI-AP) on the cell membrane surface [3–7]. Here, PIGA is linked to paroxysmal nocturnal hemoglobinuria.