Figure 3 summarizes a subset of the most significant interactions defined by this approach. These networks were further validated using siRNA-mediated knock-down of the expression of critical TF genes in AML cells. Most significantly, the AP-1 TF family formed a prominent regulatory node in all the AML subsets, and the expression of a dominant negative form of AP-1 was sufficient to block both FLT3-ITD and t(8;21) AML tumor formation in mice.12 This evidence concerns the gene TF and acute myeloid leukemia.