The development of drug resistance in AML is a tremendously complicated process involving several mechanisms, which include, for example, the up-regulation of multi-drug resistance proteins and NF-kB (which activates the PI3K/AKT/mTOR pathway), FLT3 mutations, RAS mutations (which activate the PI3K/AKT/mTOR and Raf/MEK/ERK pathways), Bcl-2 mutations, and c-Myc mutations, and modifications to pathways that regulate reactive oxygen species (ROS) signalling [11]. This evidence concerns the gene MTOR and acute myeloid leukemia.