SMAD3 and acute myeloid leukemia: In some cases of leukemia, resistance to TGF-β-induced cytostatic effects was correlated with the activation of oncogenic transcription factors,17 for example, Runx1-ETO in acute myeloid leukemia (AML)18 and PML-RARα in acute promyelocytic leukemia (APL) and Evi-1 in chronic myeloid leukemia (CML).3 Amplified Evi-1 in CML interacts with Smad3 and disrupts Smad3-DNA binding, leading to repression of TGF-β signaling in the blast phase of CML.19 Therefore, oncogene-mediated blockade of TGF-β signaling might be an alternative way for cancer cells to escape TGF-β tumor suppressor signaling.