To address whether Dlx5 itself could represent a direct driving force in T-ALL, and how epigenetic reprogramming via a homeobox gene might contribute to T-lymphomagenesis generally, we generated a transgenic mouse model with thymocyte-specific overexpression of Dlx5, and we found that these Lck-Dlx5 mice develop thymic lymphomas with high penetrance. The gene discussed is LBX1; the disease is acute lymphoblastic leukemia.