KL and chronic myelogenous leukemia, BCR-ABL1 positive: Under EPO deprived conditions, we observed marked inhibition of CML erythroid colony growth by several potent inhibitors of Bcr-Abl [25], thus providing evidence that Bcr-Abl increased Tyrosine Kinase activity cooperates with KL and other cytokine activated pathways in early CML progenitors to reprogram and distort their direction of lineage commitment, which in normal bone marrow and mobilized peripheral blood progenitors, and to a lesser extent in cord blood cells, is more dependent on EPO for production of erythroid cells.