Trimova G, Yamagata K, Iwata S, et al. - The source of 14-3-3η was investigated by immunostaining RA synovial tissue. Researchers evaluated source of 14-3-3η by immunostaining RA synovial tissue. They selected fibroblast-like synoviocytes, CD4+ cells, and macrophages as candidates among the various cell types in the synovial tissue. They examined phosphorylation of mixed-lineage kinase domain-like pseudokinase (MLKL) and cell death of macrophages by phalloidin staining and electron microscopy after stimulation with oxidative stress inducer (diamide) or tumour necrosis factor (TNF)-α. The western blotting examined extracellular 14-3-3η protein levels. The outcomes indicated that macrophages that highly express 14-3-3η undergo TNF-α-induced necroptosis with damage to the cellular structure, appearing in the secretion of 14-3-3η into the extracellular space. This study found a new tool for 14-3-3η level improvement in the RA synovial fluid.