Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, life-threatening acquired hematopoietic stem cell disorder resulting from the somatic mutation of the X-linked phosphatidylinositol-glycan complementation class A (PIG-A) gene (1–4). In normal individuals, this gene encodes an enzyme involved in the first stage of glycophosphatidylinositol (GPI) biosynthesis. In PNH, as a result of the mutation(s) in the PIG-A gene, there is a partial or absolute inability to make GPI-anchored proteins, including complement-defense structures such as CD55 and CD59 on red blood cells (RBCs) and white blood cells (WBCs) (5–8). Absence of CD59 in particular (9, 10) and CD55 on RBCs is largely responsible for intravascular hemolysis associated with clinical PNH (reviewed in reference 11).