Recent evidence highlightsthe contribution of endoplasmic reticulum (ER) stress in the pathogenesis and treatment of RA.Herein, we study the expression of the ER stress sensor inositol-requiring enzyme 1α (IRE1α),as well as XBP1 splicing and the regulated IRE1-dependent decay (RIDD), in peripheral bloodmononuclear cells (PBMCs) from patients with RA compared with healthy controls. The gene discussed is XBP1; the disease is rheumatoid arthritis.