Upregulation of EPOR in the IPS model also recapitulates what is seen in patients with ETV6-RUNX1+ ALL (Torrano et al., 2011); more broadly we see upregulation of a battery of myeloid cytokine regulators, the functional relevance of which is clearly demonstrable by the markedly increased cloning frequency and residual myeloid potential of ETV6-RUNX1+ “proB” cells in response to myeloid cytokines (Figures 6F–6G), a feature reminiscent of the lineage promiscuity characteristic of cALL. This evidence concerns the gene RUNX1 and acute lymphoblastic leukemia.