In intestinal metaplasia, levels of key modulators of the UPR activated by ER stress such as HSPA5 (encoding for binding immunoglobulin protein; BiP), C/EBP-homologous protein [CHOP; positively controlled by the protein kinase R (PKR)-like ER kinase (PERK) pathway], and XBP1 (downstream of inositol-requiring enzyme-1 alpha; IRE1-α), were reportedly higher in H. pylori-positive subjects compared to earlier precancerous stages (i.e., non-atrophic and atrophic gastritis) (Baird et al., 2013). The gene discussed is HSPA5; the disease is chronic atrophic gastritis.