One study reported that when human embryonic stem cell-derived mesenchymal stem/stromal cells (hES-MSCs) were in direct contact with brain microvascular endothelial cells (BMECs), TNF-α-induced changes in tight junction proteins, permeability, trans-endothelial resistance, and adhesion molecule expression were reversed, thereby repairing the neuroinflammation-associated BBB damage accompanying experimental autoimmune encephalomyelitis (EAE) [44]. The gene discussed is TNF; the disease is experimental autoimmune encephalomyelitis.