HBG1 and sickle cell disease: CRISPR-Cas9 editing in both HUDEP-2 cells and CD34+ progenitors from patients with sickle cell anemia generated small deletions disrupting the binding motifs for: ZBTB7A 195–197 bp upstream of both HBG2 and HBG1; the BCL11A binding motif 115 bp upstream of both HBG2 and HBG1; and the QTL 158 bp upstream of HBG2. These induced mutations mimicked HPFH mutations (Table 2).