Create a compound motif of GATA1 and TAL1 in the non-coding region of the HBZ gene to reactivate zeta-globin

alpha-thalassemia is one of the most prevalent hereditary blood disorders; however, effective gene therapies for this condition are currently lacking. zeta globin, an embryonic alpha like globin, can combine with beta-like globin to form a tetramer of Hb Portland2 , which alleviates the symptoms of alpha-thalassemia. The use of CRISPR-Cas9 technology and single-stranded oligodeoxynucleotide (ssODN) as a template chain enabled the modification of a limited number of bases through homology-directed repair (HDR), resulting in the creation of a GATA1 TAL1 complex binding site within the non-transcribed region of HBZ.This part is RNA-SEQ data from undifferentiated CD34 cells.