We initially assumed that the transactivation of the TetO-Stat5 transgene by the MMTV-tTA might not have been efficient enough, and we, therefore, crossed both TetO-Stat5 responder lines with Eμ-tTA and Tal1-tTA transgenics that have been utilized to generate multiple leukemia and lymphoma models [40], [41]. The gene discussed is TAL1; the disease is lymphoma.