With this direct coupling of mitochondrially generated ATP to incoming glucose via VDAC1-bound HK, mitochondria regulate glycolytic flux with that of the tricarboxylic acid (TCA) cycle and ATP synthase to balance the energy requirements of the tumor cell with biochemical requirements for metabolites (i.e., the anaplerotic and cataplerotic pathways, respectively) or metabolite precursors that are required by the tumor (Pedersen et al., 2002; Mathupala et al., 2006; Pedersen, 2007; Shoshan-Barmatz et al., 2010). The gene discussed is HK1; the disease is neoplasm.