The reprogramming of energetic metabolism in tumour cells is mainly driven by the deregulation of the nutrient‐sensing pathways.14 The occurrence of mTORC1 constitutive activation independent of PI3K/AKT and the additional possibility of AMPK activation illustrates the complexity of the interactions between the nutrient‐sensing pathways in the AML context (reviewed in Ref15, 37). This evidence concerns the gene AKT1 and neoplasm.