Whereas mutations of components involved in AKT downstream signaling are rarely found in AML, mutations of membrane-bound proteins upstream of AKT that trigger its activation are common.28 A frequent source of AKT deregulation in AML are mutations in receptor tyrosine kinases such as presence of FLT3-ITD38 or aberrant IGF1/IGF1-R signaling.39 Compounds that interfere with AKT signaling are currently used for AML therapy; however, further understanding of this pathway in order to improve drug development is still needed. Here, IGF1R is linked to acute myeloid leukemia.