These include ligand independent activating mutations of Flt3, cKit, MPL [8], and chromosomal translocations giving rise to constitutively active fusion proteins such as AML1/ETO in AML, PML/RARα in acute promyelocytic leukemia (APL), BCR/ABL in chronic myeloid leukemia (CML) [9], and the FGFR1 and PDGFR fusion partners which include ZNF198-FGFR1, FIPILI-PDGFRα and ETV6-PDGFRβ involved in chronic eosinophilic leukemia (CEL), juvenille myelomonocytic leukemia (JMML) and chronic myelomonocytic leukemia (CMML) [10,11]. This evidence concerns the gene ABL1 and acute promyelocytic leukemia.