In fact, we propose that mitochondrial oxidative phosphorylation may be important in supporting HCC cell proliferation based on the following observations: 1) the content of lactate, the major end product of glycolysis, is lower in JHH7 cells than in Hc cells (0.40-fold, Table S2) and 2) ACR up-regulates the expression of PDK4, which attenuates the flux of glycolytic carbon into mitochondrial oxidation and can reduce the production of ATP and inhibit the growth of JHH7 cells. The gene discussed is PDK4; the disease is hepatocellular carcinoma.