As it was discussed previously, a GC resistant phenotype in ALL possesses efficient mechanisms for a rapid adaptation to glycolysis inhibition, caused by GCs, by a switch to mitochondrial OXPHOS, with an up-regulation of both glycolysis and mitochondrial metabolism (see section Metabolic Re-programming and Upregulation of the PI3K/Akt/mTOR Pathway Is Related to GC Resistance in ALL). This evidence concerns the gene AKT1 and acute lymphoblastic leukemia.