In AD, ER stress is critical in determining disease progression, as it activates the UPR to restore ER homeostasis.[62] However, excessive stress can impair mitochondrial function, promote inflammation, and trigger programmed cell death of neurons.[26, 62, 63] The core proteins that initiate this evolutionarily conserved response in mammalian cells are ATF6, PERK, and IRE‐1α.[64] We found that miR‐7670‐3p, which targets ATF6, was upregulated in exosomes secreted by BV2 cells and brain tissue after 1070‐nm light irradiation. This evidence concerns the gene ATF6 and Alzheimer disease.