Lastly, we suggest that GAB2 and its effectors, including its druggable target gene products AXL and GFRA2/RET, should be further pursued as potential prognostic markers and therapeutic targets in AML, which could be achieved by various strategies: First, drugs in (pre)clinical development blocking the SHP2, PI3K and STAT5 axes, could be used to indirectly counteract GAB2-mediated amplification of FLT3-ITD signaling. Here, FLT3 is linked to acute myeloid leukemia.