The reprogrammed macrophage-like cells (termed MLCs) had increased expression of myeloid master regulators C/ebp-α and Pu.1, and corresponding overexpression of C/ebp-α and Pu.1 significantly induced myeloid reprogramming, suggesting that the myeloid cytokines and myeloid transcription factors cooperate to confer a myeloid cell fate to B-ALL, consistent with the ability of these two transcription factors to confer a myeloid fate to lymphocytes (11, 12, 14). The gene discussed is SPI1; the disease is precursor B-cell acute lymphoblastic leukemia.