IL-7 is a cytokine that plays a central role in the development, survival and proliferation of T and B cell lymphocytes. Overexpression of IL-7 in mice (Tg IL-7) leads to both increased proliferation of early T and B cell progenitors and T and B cell lymphomas. Genetic evidence indicates that known IL-7 receptor (IL-7R)-dependent proteins, including pro-survival protein Bcl-2, may not be solely responsible for the effects of IL-7. Other studies indicate that known IL-7-induced signaling proteins dock to a specific tyrosine (Y449) residue on the IL-7R. We have previously shown in a IL-7Ra^449F knock-in model that IL-7-induced lymphomas require Y449 phosphorylation and loss of this phosphorylation confers protection from disease. However, the mechanism by which this lymphoma protection occurs remains unclear. Using this genetic model, we aimed to identify novel pro-survival factors important for IL-7-mediated lymphocyte development and lymphomagenesis. An iTRAQ proteomic analysis was performed comparing CD4^-CD8^- double negative T cell progenitors from mice overexpressing IL-7 (Tg IL-7) (lymphoma prone) to Tg IL-7 mice with a mutated IL-7 receptor (Tg IL-7//IL-7Ra^449F) (lymphoma protected). Several proteins involved in survival/proliferation and apoptosis were found to be differentially expressed between the two samples and three proteins of particular interest, Gimap4, Bit1 and FKBP 51 were validated by immunoblot analysis.