As leukemia models, we chose: (i) the knock-in (KI) model of t(15;17) AML, in which the PML-RARα fusion gene is expressed from the murine cathepsin G gene promoter (PR, [7]), and (ii) the t(8;21) AML, in which the full length AML1-ETO gene fusion is cloned within the endogenous Aml1 locus and expressed upon Cre-mediated recombination (AE, [8]). The gene discussed is RUNX1T1; the disease is acute myeloid leukemia.