In conclusion, since VDAC1-bound HK is essential for tumor cells, conferring several advantages (see HK-linked Protection Against Cell Death is Mediated via Interaction with VDAC1), including protection against apoptotic events and promoting aerobic glycolysis, the detachment of HK from VDAC1 offers a novel therapeutic strategy to augment apoptosis, revert the hyper-glycolytic state and enhance the therapeutic efficacy of conventional chemotherapeutic agents. The gene discussed is HK1; the disease is neoplasm.