Hyperphosphorylation of eEF2 has been demonstrated in AD brain samples, and we reported recently that suppression of eEF2K and eEF2 phosphorylation could alleviate synaptic failure and cognitive deficits in AD model mice without affecting the brain amyloid beta (Aβ) pathology.25, 26. The gene discussed is EEF2; the disease is Alzheimer disease.