Notably, constitutive activation of AKT (indicated by increased phosphorylation of AKT on Ser473 and Thr308) is found in 50–70% of AML patients.34 Multiple studies in the course of the last years demonstrated that aberrant activation of AKT signaling plays a critical role for the survival and maintenance of AML cells (reviewed in Fransecky et al.,35 Park et al.36 and Birkenkamp et al.37). The gene discussed is AKT1; the disease is acute myeloid leukemia.