||The study of metabolism is fundamental to understanding the basis of disease. Subtle differences in metabolites, and shunting of molecules from one pathway to another can have profound effects on cellular physiology. In the case of cancer cells this metabolic balance is often severely disrupted. Many cancer cells rapidly consume glucose to produce pyruvate, but rather than entering the mitochondria for oxidation, it is reduced to lactate and excreted from the cell. This phenomenon is known as the "Warburg effect" and provides the cell ample biosynthetic precursors for proliferation, many of which are side-reactions of glycolysis. Similar to cancer cells, stem cells also place a heavy metabolic emphasis on glycolysis. During the process of differentiation, however, stem cells shift their metabolic profile towards oxidative phosphorylation and mitochondrial respiration. Unlike stem cells, many cancer cells are limited in their ability to adapt to a different, more oxidative metabolic regime. In both cancer cells and stem cells, the fate of pyruvate is tightly controlled. The mitochondrial pyruvate carrier (MPC), a heterodimeric protein complex, is required for pyruvate import into the mitochondria. The recent discovery of the genes encoding the MPC have provided a new lens to evaluate pyruvate metabolism in normal and disease physiology. Herein, the role of the MPC and its connection to the Warburg effect are described in the context of normal physiology, colon cancer, and resident colon stem cells.