The high AMP and low ATP concentrations in Hepa-c4 tumours suppressed the normal inhibition of phosphofructokinase-1 (PFK-1, the main control enzyme in the glycolytic pathway) by ATP, and allowed it to be allosterically activated by AMP [18], thus explaining the normal glucose uptake and glycolysis in Hepa-c4 cells under both normoxia and hypoxia. The gene discussed is PFKM; the disease is neoplasm.