Accumulating evidence indicate that mutations in the FLT3 gene are disease promoting rather than disease initiating events [111,112], and that mutant FLT3 cooperates with other oncogenes and aberrantly regulated proteins associated with AML, e.g., NPM1, DNMT3A [19], NUP98/NSD1 [113] DEP-1, PML-RAR and AXL [114,115,116]. This evidence concerns the gene PRAM1 and acute myeloid leukemia.