T cell Acute Lymphoblastic Leukemia (T-ALL) is a highly heterogeneous hematological malignancy resulting from the transformation of immature thymocytes during their development. Despite this heterogeneity, there are several recurring mutations fond in the majority of T-ALL patient. 60% of all pediatric T-ALL patients have mutations in the TAL1 gene, and 10% of have mutations in the related LYL1 gene. TAL1 and LYL1 are transcription factors typically expressed in hematopoietic progenitors that form complexes with the transcription factor E2A, which then recruits other factors including the LMO proteins, LDB1, and GATA proteins. This complex regulates numerous functions in hematopoietic progenitors, including quiescence, self-renewal, and antagonizes lymphoid development. In the thymus, TAL1 and LYL1 expression is extinguished as thymic progenitors receive T cell lineage specifying signals and commit to the T cell lineage. As TAL1 and LYL1 expression is extinguished, E2A dimerizes with another transcription factor, HEB, to enforce the T cell lineage and promote healthy T cell development. One major oncogenic function of ectopic TAL1/LYL1 expression is the inhibition of these E2A:HEB dimers and the repression of the T cell lineage specifying function of E2A. Indeed, mouse models that ectopically express the inhibitors of E2A DNA binding, the ID proteins, or delete E2A in the germline faithfully recapitulate many features of human TAL1+ T-ALL. I use multiple mouse models that delete E2A at different stages of T cell development to investigate the different functions of E2A and how these functions contribute to the suppression of T-ALL. Deleting E2a at the hematopoietic stem cell stage was sufficient to induce robust leukemogenesis, while deleting E2a at the DN2/DN3 stage was only weakly oncogenic. Additionally, only early deletion resulted in the upregulation of the T-ALL-associated pathways Notch, Wnt/β-catenin, NFκB, and Myc. Further, the early deletion induced developmental defects in the thymocytes, which resulted in a 3-5 fold decrease in the number of thymocytes at 3-5 weeks of age. This reduction in the number of thymocytes in the early deletion correlates with an inability of thymocytes to provide a competitive environment. Further, the later deletion showed no signs of impaired competition, and restoring competition in the early deletion was sufficient to significantly inhibit leukemogenesis. Restoring competition induced several transcriptional changes in the E2A deficient thymocytes, most notable of which were an inhibition of the Myc pathway and an induction of apoptotic pathway genes. Overall, my analysis provide insight into how the stage at which the tumor suppressor E2A differentially predisposes thymocytes to transformation and how early deletion promotes leukemogenesis through induction of oncogene activation and rendering thymocytes unable to out compete pre-leukemic cells.