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Moreover, we found that the K562-28(AG) cell line is more sensitive to hypoxia and shows a defective erythrogenic program compared with K562 before differentiation. Importantly, all abovementioned abnormalities in K562-28(AG) were reversed after correction of this mutation with CRISPR/Cas9 and assODNs, confirming the specificity of these phenotypes. Overall, this is the first time to analyze the effects of the HBB -28(AG) mutation at the whole-transcriptome level based on isogenic cell lines, providing a landscape for further