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Recently, we observed that common genetic variants associated with fetal
haemoglobin (HbF; a2c2) level and b-haemoglobin disorder clinical
severity mark an adult-developmental-stage- and erythroid-lineage-specific intronic enhancer of BCL11A (ref. 28), a validated repressor of HbF
and therapeutic target for b-haemoglobin disorders28,31–33. This composite human enhancer is composed of three DNase I hypersensitive sites
(DHSs), termed h155, h158 and h162 on the basis of distance in
kilobases (kb) from the transcriptional start site (TSS)28. The most highlytrait-associated haplotype is defined by two single nucleotide polymorphisms (SNPs): rs1427407 within h162 and rs7606173 within
h155 (Extended Data Fig. 1a)
1 answer
Common genetic variants linked to fetal hemoglobin levels and beta-hemoglobin disorder severity are associated with an intronic enhancer of the BCL11A gene, which is a known repressor of fetal hemoglobin and a target for beta-hemoglobin disorders.