We therefore surmised that chromosomal translocations or retroviral integration upstream of the LMO2 locus observed in pediatric T-ALL overcome these repressive marks to cause ectopic expression of oncogenes such as LYL1, SCL and LMO2 which, in the context of DN3 thymocytes, collaborate with NOTCH1-HES1/MYC to confer aberrant self-renewal to these cells. This evidence concerns the gene LYL1 and acute lymphoblastic leukemia.