The serine/threonine kinase mTOR complex 1 is overactivated in the majority of AMLs and promotes glycolysis in these cells and drives glycolysis addiction; mTOR inhibition induces metabolic reprogramming in AML cells; metabolic analysis showed an important role of glucose-6-phopshate dehydrogenase (G6PD) and of the pentose phosphate pathway in sustaining the energetic metabolism of leukemic cells [86]. The gene discussed is G6PD; the disease is acute myeloid leukemia.