In conclusion, the animal models have been of fundamental importance in defining the oncogenic activity of FLT3-ITD mutations in the context of various genetic models of AML in mice, particularly for: (a) demonstrating that FLT3-ITD alone does not fully transform a cell to leukemia, while the combination of FLT3-ITD with other oncogenic mutations can lead to the development of a full-blown leukemia in mice; (b) elucidating the molecular mechanisms underlying deregulated growth induced by FLT3 mutants; (c) developing robust in vivo platforms for discovery of new FLT3 inhibitors. Here, FLT3 is linked to leukemia.