Since we show that Gab2, as an important Flt3-ITD effector, increases Axl expression and, as discussed, AXL in turn promotes FLT3-ITD signaling, we propose a self-sustaining feed-forward loop with a central role for Gab2 in enhancing the oncogenic signals of Flt3-ITD and contributing to AML aggressiveness (Fig. 8). The gene discussed is GAB2; the disease is acute myeloid leukemia.