Our observation of SCL/TAL1 binding to the LMO1 +57 enhancer now provides for the first time, evidence for a direct cross-regulatory link between SCL/TAL1 and LMO1, two leukaemia oncogenes known to collaborate during T-ALL development in mouse models.7, 9 A model is therefore emerging whereby high levels of SCL/TAL1 might contribute to the ectopic expression of LMO1, which in turn would serve to enhance the leukaemogenic function of SCL/TAL1 and thus provide a clonal advantage to SCL/TAL1-expressing preleukaemic T-ALL cells that activate expression of LMO1. The gene discussed is LMO1; the disease is acute lymphoblastic leukemia.