The interaction of HK1 or HK2 with VDAC1 gives numerous advantages to cancer cells: (1) it mediates the increased permeability of the OMM to adenine nucleotides; (2) it increases the rate of aerobic glycolysis and thereby allows the cells to adapt to hypoxic conditions; (3) it mediates elevated resistance to apoptosis and protection from oxidative stress as VDAC1-bound HK acts as an anti-apoptotic protein (73, 87–89). The gene discussed is VDAC1; the disease is cancer.