AKT1 and acute myeloid leukemia: Internal tandem duplication (ITD) in the juxtamembrane portion of FMS-like tyrosine kinase-3 (FLT3) is one of the most prevalent molecular alterations in acute myeloid leukemia (AML).1 FLT3-ITD mutations cause constitutive activation of FLT3 signaling and its downstream signaling pathways, including MAPK/ERK, JAK/STAT5, and PI3K/AKT, resulting in uncontrolled proliferation, inhibition of differentiation, and reduction of apoptosis in AML cells.2 AML patients with FLT3-ITD mutations present with high relapse rates and poor overall survival.3,4