This transposase-based integration system achieved stable fetal γ-globin expression in CD46-transgenic and thalassemia mouse models.92–94 This method when tested in rhesus macaques demonstrated stable HSC transduction, thereby improving its feasibility in human HSC gene therapy.95 Besides thalassemia, this approach has been recently used to correct the sickle cell phenotype. This evidence concerns the gene CD46 and thalassemia.