A similar contradictory metabolic scenario was already reported in myoblasts in response to amino acids.53 The authors proposed that the concurrent activation of AMPK and mTORC1 is implicated in the maintenance of protein homoeostasis and on the fuel of metabolites for biosynthetic processes.53 The relevance of amino acid signalling and mTORC1 PI3K/AKT‐independent activation in the context of AML remains to be explored. This evidence concerns the gene AKT1 and acute myeloid leukemia.