Zhang et al. observed that EVs isolated from synovial fibroblasts of patients with rheumatoid arthritis carried a transmembrane form of TNFα, which was able to activate the NF-κB pathway and induce MMP-1 expression in fibroblast cultures, and to promote proliferation and resistance to apoptosis when added to CD4+ T lymphocyte cultures, suggesting that TNFα in the EVs could be contributing to joint inflammation[30]. The gene discussed is TNF; the disease is Arthritis.