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False-colored scanning electron micrograph of erythrocytes
7 a+ d0 O1 p% z! [ u9 ^( V- s(diameter ~7 micrometers). Sickle cell disease results from an
" g. I5 n! L6 V& G9 C6 linherited defect of adult hemoglobin, the oxygen-carrying
* ^1 i+ q% E/ X) P: zmetalloprotein constituent of erythrocytes. Common genetic variation
6 Q s5 Y4 o, ~# m6 o, Iassociated with sickle cell disease severity modulates an adult-stage
5 ~' R' c% ]: [' terythroid enhancer element of the BCL11A gene. Disruption of this& ~6 w! O. e- ~2 v
element could ameliorate the disease by reestablishing expression
- |, C9 b% Q- G2 Hof fetal hemoglobin. See pages 206 and 253.
! |# g$ `8 S) c R0 Q& j* c; H+ v
7 \, p8 ^) C3 \! G9 P
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