In rheumatoid arthritis (RA), overproduction of the cytokine tumor necrosis factor (TNF) is a central event in pathogenesis, and endoplasmic reticulum (ER) rich T cells are the major releasers of TNF in inflamed joints.108,109 Wu et al. found that the abundance of mitochondrial Asp in T cells in rheumatoid arthritis (RA) was decreased, which inhibited NAD+ turnover, resulting in a decrease in NAD+/NADH ratio and a reduction in ADP-ribosylation of proteins which is NAD+ dependent. This evidence concerns the gene TNF and rheumatoid arthritis.