This discrepancy may be related to the unfolded protein response (UPR) (Ismael et al., 2021): UPR upregulates CHOP via the PERK/eIF2α/ATF4 pathway (Hetz and Mollereau, 2014), with activation occurring in the early stages of neurofibrillary degeneration (Hoozemans et al., 2009), while the GSE5281 samples represent late-stage AD pathology (Braak stages V-VI) (Miller et al., 2008). This evidence concerns the gene EIF2AK3 and Alzheimer disease.