It has been shown that induction of HBA2 deletion in human HSPC using CRISPR/Cas9 can reconstruct α‐thalassemia traits downregulate α‐globin expression, and subsequently improve β0‐thalassemia phenotypes by targeting the endogenous HBA promoter to combine the deletion of HBA2 with the gene replacement of HBB to increase β‐globin gene expression.287. Here, HBA2 is linked to alpha thalassemia spectrum.