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Human genetics implicates a BACH2–NRF2 axis in fetal haemoglobin activation
Abstract Human genetic studies have identified key regulators of fetal haemoglobin (HbF) expression, including BCL11A, resulting in therapeutic advances1,2,3,4,5,6,7,8. Yet the mechanisms by which HbF expression is activated remain incompletely understood9. Here we conduct a large multi-ancestry genome-wide association study of HbF levels in 28,279 individuals that identifies 91 conditionally independent associations across 12 genomic regions.
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