Triggers of ER stress include gene mutations, oxidative stress, viral infections, diabetes, malnutrition, and drug toxicity.In response to these stressors, ER sensors—PERK(Protein Kinase RNA-like Endoplasmic Reticulum Kinase), IRE1(Inositol-Requiring Enzyme 1), and ATF6 (Activating Transcription Factor 6)—detect the build-up of unfolded proteins, activating the UPR to reduce ER burden through mechanisms like reduced protein synthesis, enhanced protein folding, and increased degradation of misfolded proteins [25–28]. The gene discussed is ATF6; the disease is viral infectious disease.