Overexpression of the last eight aa of HKDC1 at the C-terminal (HKC8) truncates significantly suppresses tumor growth and results in dissociation of HKDC1 from vascular endothelial growth factor 1 (VDAC1), indicating that HKC8 may be a novel antitumor target for ENKTL treatment. This evidence concerns the gene VDAC1 and neoplasm.