Enhanced glycolysis has been observed in AML cell lines and in human primary AML blasts [10], while both the phosphoinositide 3-kinase (PI3K)/serine-threonine protein kinase B (AKT) and the mammalian target of rapamycin (mTOR) seemingly contribute to this glycolytic metabolism [11,12]. Here, MTOR is linked to acute myeloid leukemia.