With the decrease of HK-2 in mitochondria, the interaction between HK-2 and VDAC was disrupted, which resulted in dramatic increase of membrane permeability and release of pro-apoptotic enzyme, such as cytochrome C. Bax in cytoplasm was significantly decreased after chrysin treatment, but Bax located on mitochondria was substantially increased, implying that the majority of Bax was transferred from cytoplasm to mitochondria after HCC cells exposed to chrysin. This evidence concerns the gene HK2 and hepatocellular carcinoma.