In this study we interrogated the roles of the major oncogenic signaling pathways downstream of Ras – PI3K, MAPK, and RALB – in AML using a tetracycline-repressible NRAS(V12) and Mll-AF9-driven mouse model (tNM AML) [23], human AML cell lines, and primary patient samples. This evidence concerns the gene NRAS and acute myeloid leukemia.