They observed that AML-microvesicle-treated NK cells underwent a significant impairment of their cytotoxic activity and reduction in the expression of the activating receptor NKG2D and that this effect was mediated by the expression of TGFβ on the surface of AML-derived microvesicles, since it could be reversed by anti-TGFβ monoclonal antibodies [50]. This evidence concerns the gene TGFB1 and acute myeloid leukemia.