The earlier onset and greater penetrance of AML development in the Combi-tTA-Snai1 mice, as well as the lack of lymphoma formation in the hematopoietic-restricted model generated by Carmichael et al., suggest that either expression level differences between the two models (which is unknown at this time) or the non-hematopoietic expression of transgenic SNAI1 in the Combi-tTA-Snai1 mice contributes to AML and/or lymphoma development. This evidence concerns the gene SNAI1 and acute myeloid leukemia.