On the other hand, Perk activation also leads to the phosphorylation of NF‐E2‐related factor 2 (Nrf2) which drives the anti‐oxidant capacity and restricts the immunostimulatory response.[11] In consideration that Ca2+ dyshomeostasis is reversible in the early stages of Aβ pathology,[10] one may reasonably deduce that a targeting therapy restoring the Ca2+ homeostasis is likely a potent means for treating AD. The gene discussed is EIF2AK3; the disease is Alzheimer disease.