We recently reported that the glycolytic inhibitors 2-DG and lonidamine activated protein kinase B (Akt) and extracellular-signal regulated kinases (ERK) in AML cells, representing a defensive response which reduces drug lethality, but they caused drug-dependent differential effects (either inhibition or activation) on the of LKB-1/AMPK pathway [21], [22]. The gene discussed is AKT1; the disease is acute myeloid leukemia.