In patients with rheumatoid arthritis, a shortage of T‐cell mitochondrial aspartate disrupted the regeneration of the metabolic cofactor nicotinamide adenine dinucleotide (NAD), causing ADP deribosylation of the endoplasmic reticulum (ER) sensor GRP78/BiP (HSPA5), the master regulator of the ER stress response [10, 11]. The gene discussed is HSPA5; the disease is rheumatoid arthritis.