Exosomes originating from leukemic cells in AML patients have a distinct molecular profile when compared to healthy individuals.(14) In addition to conventional markers for exosomes such as tetrapanins, AML exosomes contain TGF-β1, MICA/MICB, FasL, and markers of myeloid blast cells (CD33, CD34, and CD117).(14)Ex vivo, these exosomes decrease NK cell cytotoxicity by decreasing expression of NKG2D.(14) In addition, TGF-β1 is partially responsible for NK cell dysfunction in AML. This evidence concerns the gene TGFB1 and acute myeloid leukemia.