A partial understanding of the pathophysiology of sickle cell disease has suggested one means of treatment-increasing the distribution and concentration of fetal hemoglobin in sickle erythrocytes. Although this can be accomplished clinically with drugs like hydroxyurea, a complete understanding of the molecular and cellular basis of fetal hemoglobin regulation may suggest new and better ways of attaining this goal.
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Martin H. Steinberg (2001) studied this question.
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