CD34 and hereditary disease: In this study we present clonal data for single-nuclease genome disruption of aberrant regulatory elements (DARE) and functional restoration of aberrant splicing in HBBIVSI-110(G>A) β-thalassemia at the DNA, RNA, and protein level, show significant correlation of findings in the utilized MEL-HBBIVS cell model with our published data in CD34+ cells, and extrapolate our findings to additional β-thalassemia mutations and prominent mutations in other genetic diseases.