Transgenic mice expressing a constitutive activation of the Akt2 oncogene specifically in immature T-cells, Lck-MyrAkt2 mice, develop a high rate of spontaneous thymic lymphomas, including some founders that acquire a recurring chromosomal inversion that juxtaposes the enhancer of the T-cell receptor-β (Tcrb) locus and the Dlx5/6 bigene, thereby, resulting in overexpression of Dlx5 and, to a lesser extent, Dlx6 [62] (Figure 4). The gene discussed is DLX5; the disease is thymus lymphoma.