Labeling erythrocytes with radioactive chromium (Cr51) has made possible study of the fate of normal and diseased erythrocytes.1 The ability of the spleen to sequester red blood cells has been demonstrated in numerous pathological states, the most prominent of which are hereditary spherocytosis, certain autoimmune hemolytic anemias, cirrhosis of the liver, and Gaucher's disease. In an effort to determine why some red cells are destroyed in the spleen while others are not, Harris, McAlister, and Prankerd studied the sites of destruction of red cells with both induced and naturally occurring abnormalities.2 Spherocytes produced by heating red cells for 15 minutes at 50 C and red cells whose surface lipids had been reduced by alumina were selectively sequestered in the spleen after injection. Red cells in which metabolism had been inhibited by incubation in sodium arsenate were destroyed in areas other than the spleen. An extensive series of