Of note, over-expression of HMGA2 transcripts, possibly due to disruption of the let-7 miRNAs binding sites at the HMGA2 locus, accompanied an increased expression of endogenous HbF in a patient receiving lentiviral beta-globin gene therapy for the treatment of severe transfusion-dependent beta-thalassemia [27]. The gene discussed is HBB; the disease is Beta-thalassemia.