The molecular defect in sickle cell disease is an error in the coding
for hemoglobin synthesis. All of a patient's erythrocyte precursors sh
are the genetic defect, but the patient's circulating erythrocytes are
heterogenous in their degree of deformability. Periodic removal, by s
elective filtration, of the least deformable of the circulating erythr
ocytes might prove of clinical benefit.