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Two common hemoglobinopathies, sickle cell disease (SCD) and β-thalassemia, arise from genetic mutations within the β-globin gene. A 500-bp motif termed Fetal Chromatin Domain (FCD), upstream of human ϒ-globin locus, may function as a transcriptional regulatory element driving inhibition of the ϒ-globin gene. Here, we hypothesize that the removal of this motif using CRISPR technology may reactivate the expression of ϒ-globin and subsequently restore fetal hemoglobin functionality. In this workdoi:10.21203/rs.3.rs-906377/v1 fatcat:gawhorw63beczomxjlycpblrwy