Our data showing that targeting downstream the NMDA receptors activation -such as neuronal glycolysis-, rather than the NMDA receptors themselves, shows neuroprotection strongly suggest that targeting PFKFB3 would be a suitable alternative strategy for the prevention of the deleterious effects of NMDA receptor overstimulation in stroke and related excitotoxicity-associated neurological disorders, such as, amongst others, traumatic brain injury, Alzheimer’ or Parkinson’ diseases. The gene discussed is PFKFB3; the disease is Stroke.