Studies had reported the well-established role of E2A in leukemogenesis: two fusion proteins, E2A-HLF [11] and E2A-PBX1 [12], both containing the transactivation domain of E2A and the DNA-binding domain of HLF or PBX1, could lead to pro-B cell acute lymphoblastic leukemia (ALL) in adolescents and pre-B cell ALL in children respectively [13]. This evidence concerns the gene HLF and B-cell acute lymphoblastic leukemia.