The pro-peptide and LAP forms of TGF-β1 abundantly present in isolated AML exosomes, but not NC exosomes may be ready for utilization and their processing to active TGF-β1 may be a link to TGF-β1-mediated suppression of immune cells seen in AML (4). This evidence concerns the gene TGFB1 and acute myeloid leukemia.