Treated with FD268, our studies documented the reduction of PI3K/Akt process and downregulation in the level of phosphorylated mTOR as well as its downstream targets p70S6K at Thr389 and 4EBP1 in both HL-60 and MOLM-16 cells, which is in agreement with those well-known PI3K inhibitors in treatment of AML [26, 46, 47]. Here, AKT1 is linked to acute myeloid leukemia.