PIGA mutation leads to impaired glycosylphosphatidylinositol (GPI) synthesis, resulting in the loss of GPI-anchored protein (GPI-AP) on the cell surface (such as CD59 and CD55) and the disruption of the increased sensitivity of blood cells to complement activation; the main clinical manifestations of PNH are chronic intravascular hemolysis, bone marrow failure, and high risk of thrombosis [1–3]. Here, PIGA is linked to paroxysmal nocturnal hemoglobinuria.