Oncogenic events that convert normal cells into cancer cells promote cell growth and proliferation and inactivate checkpoints that would normally block these functions in the absence of sufficient growth factor, oxygen and nutrient availability. Other oncogenic events block cell death, induce tumor vascularization, and promote genetic instability that accelerates tumor progression. Tumor cells also rewire metabolism to increase nutrient uptake, to produce building blocks for new cells, and to sustain energy homeostasis in stress and with the high metabolic demand of cell growth and proliferation. This distinct metabolism of cancer cells has been known for decades, and was first highlighted by Otto Warburg who found that cancer cells undergo aerobic glycolysis. This was termed the “Warburg effect” and is the basis for current FDG-PET imaging of tumors. Furthermore, clinically important anticancer agents include inhibitors of cellular metabolic pathways (e.g., antifolates, the thymidylate synthase inhibitor 5FU, the nucleoside analog gemcitabine). Despite this, until recently cancer metabolism was an area of little research.