Their findings reveal a characteristic molecular profile for TEXs isolated from AML patients and substantiated the role of the TGF‐β1‐Smad2/3 pathway in NKG2D downregulation, implying that the activation of this pathway in NK cells is, at least partially, responsible for the lowered anti‐tumour activity expressed by these cells in AML (Whiteside, 2013). This evidence concerns the gene SMAD2 and acute myeloid leukemia.