T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological neoplasm with poor outcome for patients with primary resistant or relapsed disease. We have identified a subset of T-ALL patients with elevated levels of SOX11, a protein that is normally not expressed in T-cells, and we also observed that SOX11 overexpression often co-occurs with stabilizing MYCN P44L mutations. Given this, we hypothesize that SOX11 might be involved in the malignant transformation of T-cells. To study this hypothesis, we developed a novel Rosa26-driven conditional knock-in mouse model with inducible overexpression of SOX11 in the T-cell lineage. Using this model, we will study potential cooperation between SOX11 activation and other genetic defects, such as overexpression of the oncogene Lmo2 or loss of the tumor suppressor Pten. Additional insights in the role of SOX11 in T-ALL might lead to the identification of novel targets for the development of less toxic treatments for T-ALL patients.