While abnormal activation of a number of genes/pathways has been implicated in the self-renewal of GMPs in myeloid blast crisis, including WNT/β-CATENIN, RUNX1, RUNX1/EVI1, RUNX1/PRDM16, GATA-2, and Msi2 [3–8], direct evidence in supporting this concept has come from studies on several genes including NUP98/HOXA9, Hes1 and Setbp1, showing that they can cooperate with BCR/ABL to transform GMPs into LICs for development of CML myeloid blast crisis in vivo [2, 9, 10]. This evidence concerns the gene SETBP1 and chronic myelogenous leukemia, BCR-ABL1 positive.