Deletion of mTOR complex-1 (mTORC1) in a T-ALL mouse model resulted in profound cell-cycle arrest and efficient eradication of T-ALL cells [10, 11], suggesting that mTORC1 can integrate signals from the PI3K-Akt and MEK–ERK signaling pathways to activate downstream components responsible for tumor cell growth and metabolism [12]. This evidence concerns the gene AKT1 and acute lymphoblastic leukemia.