All the above findings suggest an increase in the phosphorylation of mTOR and 4E-BP1 in AD mice and in patient samples, which correlate with tau protein pathophysiology, suggesting that inactivation of 4E-BP1 through phosphorylation causes eIF4E to participate in protein translation, which in turn increases the synthesis of tau protein [141]. This evidence concerns the gene EIF4EBP1 and Alzheimer disease.