Rapidly dividing tumor cells must increase ATP production and utilization in order to provide the necessary building blocks to maintain their increased biomass. Alterations in cellular metabolism thus occur in order to provide these requisite anabolic precursors. We are interested in the means by which Myc alters aerobic glycolysis and mitochondrial structure and function in vivo. We have recently shown that Myc exerts profound effects on these processes, particularly in conjunction with other proteins that sense and respond to intracellular energy levels such as carbohydrate response element binding protein (ChREBP) and AMP-dependent protein kinase (AMPK). We are currently employing a variety of mouse knockout models to define the functional relationships among these pathways and how they cross-talk with one another to balance energy production and utilization to maintain the growth of tumor cells.