We previously showed that heterozygous reduction of eEF2K partially improved spatial learning and memory deficits in an AD mouse model (Beckelman et al., 2019), leading to the hypothesis that further suppression (e.g., homozygous knockout) of eEF2K and eEF2 phosphorylation would fully restore the impairments of spatial learning and memory. The gene discussed is EEF2; the disease is Alzheimer disease.