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]. The gene discussed is ERN1; the disease is Alzheimer disease.