Recent studies have substantially supported the concept of FLT3-ITD as a valid therapeutic target in human AML, and suggested that FLT3-ITD is capable of conferring a state of ‘oncogene addiction’, whereby cellular survival pathways associated with normal or precancerous cells can become hijacked, leading to a state of reliance upon key signaling molecules that can be exploited therapeutically[24]. The gene discussed is FLT3; the disease is acute myeloid leukemia.