In contrast to solid tumors, mutations in SMAD genes are rare in leukemia and disruption of TGFβ responsiveness is commonly secondary to either (a) altered transcription, as described in acute myeloid leukemia with translocation t(8;21), in which the AML1/ETO chimeric protein represses transcription of TGFβ-responsive genes [8] or (b) disruption of TGFβ target gene expression such as the cell cycle regulators c-Myc, p15 and p21, which are commonly associated with leukemogenesis [9]. Here, TGFB1 is linked to acute myeloid leukemia.