This hematopoietic independence suggests that the program that we observed driven by TCF7L2/MYC cooperation profoundly reprograms leukemic cells during advanced phase CML and regulates a stem cell program involving pluripotent stem cell functionalities [22] shared also with an aggressive undifferentiated sub-group of hepatoblastoma [23]. The gene discussed is TCF7L2; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.