If one considers the metabolic importance of both VDAC1 and HK, the role that HK fulfills in promoting tumor cell survival and the function of the HK–VDAC1 interaction in regulating apoptosis, as well as other functions as presented above, then disruption of the HK–VDAC1 complex represents an attractive target for cancer therapy and may form the basis for novel anti-cancer drugs. The gene discussed is HK1; the disease is cancer.