Glycophosphatidylinositol-linked proteins decay accelerating factor (DAF; CD55) and membrane inhibitor of reactive lysis (MIRL; CD59) are responsible for clinical manifestations and laboratory changes associated with PNH.(5,6) These proteins protect normal red blood cells from complement-mediated lysis via prevention of C3 convertase activation and inhibition of membrane attack complex formation.(3) Blood cells with decreased CD55 and CD59 expression are therefore sensitive complement-mediated lysis, which ultimately results in clinical manifestation of the disease. This evidence concerns the gene CD59 and paroxysmal nocturnal hemoglobinuria.