Another approach to use this unique expression system would be to replace the strong SFFV promoter with weaker options, e.g., WT1’s endogenous or a regulatable promoter, and then to study the effect of WT1 overexpression on leukemogenesis, differentiation and chemotherapy resistance in normal CD34+ progenitor cells that additionally co-express other type I or type II mutations detected in AML blasts. This evidence concerns the gene WT1 and acute myeloid leukemia.