Similarly, the simultaneous inhibition of glycolysis with 2-DG or lonidamine, and of FAO with etomoxir, enhances the anti-cancer effect of arsenic trioxide (AsO) in acute pro-myelocytic leukemia cells [219]: the mechanism is related to a significant drop in ATP levels and to a down-regulation of the pro-survival ERK1/2 and Akt-dependent pathways. Here, AKT1 is linked to cancer.