In the AD brain, the continuous accumulation of Aβ and hyperphosphorylated Tau leads to the continuous increase of endoplasmic reticulum stress (ERS), which sequentially activates the unfolded protein response (URP) and NF-κB, through the PKR-like ER kinase (PERK)/JAK1/STAT3 and inositol-requiring enzyme 1 (IRE1)/thioredoxin-interacting protein (TXNIP) signal pathways, thereby causing aseptic inflammatory responses [132, 133]. This evidence concerns the gene EIF2AK3 and Alzheimer disease.