HMGA2 and thalassemia: In the case reported in 2010 by Cavazzana et al. of an adult patient with severe βE/β0-thalassaemia treated with gene therapy, the presence of a dominant, myeloid-biased cell clone was demonstrated, in which the integrated vector transferring the β-globin gene caused the transcriptional activation of HMGA2 in erythroid cells and further increased the expression of a truncated HMGA2 mRNA insensitive to degradation by let-7 miRNAs [94].