Notably, the authors showed that the genetic reduction of eEF2K partially rescued this deficit in protein translation, and reversed cognitive and long-term potentiation (LTP) deficits of two distinct AD mouse models (Tg19959 and APP/PS1), thus revealing the role of translational dysregulation caused by abnormal eEF2 phosphorylation in AD. This evidence concerns the gene EEF2K and Alzheimer disease.