Two of the four primary T-ALLs with LMO1 enhancer mutation harboured SIL-TAL1 deletion and one carried TCR-TAL2 translocation (Supplementary Table S2), indicating that they belong to the TAL1/TAL2+ molecular subtype of T-ALL, consistent with the notion that TAL and LMO proteins act as a complex and function cooperatively in T-ALL transformation.30, 31 None of these four cases had characteristics of early T-cell precursor (ETP) ALL, in that the TCRγ chain was rearranged in the three cases that were tested and the immunophenoytpe of each case did not meet the criteria for ETP ALL.32, 33. The gene discussed is TAL2; the disease is acute lymphoblastic leukemia.