LMO2 is an oncogenic transcription factor that is frequently overexpressed due to chromosomal abnormalities in T-cell acute lymphoblastic leukemia (T-ALL). In transgenic mouse models, LMO2 overexpression causes thymocyte self-renewal resulting in T-cell leukemia with long latency. However, the requirement for LMO2 for leukemia maintenance is poorly understood. To study this, we developed a Tetracycline-regulated knock-in mouse model that reversibly expresses LMO2 throughout the haematopoietic system. This led to a specific impairment of T-cell development and the development of self-renewing preleukemic stem cells (pre-LSCs) in the thymus. This was followed by the development of fully penetrant T-lymphoblastic leukemia resembling human T-ALL. In preleukemic mice, repression of LMO2 overcame the LMO2-induced thymocyte developmental block, reversed LMO2-induced gene expression changes and eliminated self-renewing pre-LSCs in vivo. Surprisingly however, the majority of LMO2-induced T-cell leukemias and leukemia-derived cell lines could be maintained in the absence of LMO2, implying an evolution of oncogene addiction that overcomes the requirement for LMO2. Leukemias that were LMO2-dependent expressed an immature gene expression profile similar to human Early T-cell Precursor-like ALL (ETP-ALL), but could not be predicted by assessment of immunophenotype or Notch pathway activation. The regulatable model used here will be useful to determine the molecular features associated with LMO2-dependence, along with critical components of LMO2-dependent and –independent self-renewal pathways in T-ALL.