These effects are largely due to the paracrine activity of MSCs, secreting factors such as transforming growth factor beta (TGF-β), nitric oxide (NO)—which modulates to prevent T-cell division by interfering with their signals, prostaglandin E2 (PGE2)—which facilitates attenuation by cutting pro-inflammatory cytokines and directing macrophages to a subdued M2 type, or indoleamine 2,3-dioxygenase (IDO) as a response to the GVHD-related elevation of pro-inflammatory cytokines including interferon gamma (IFN-γ), tumor necrosis factor alpha (TNF-α), or interleukin 1β (IL-1β) [14]. The gene discussed is TNF; the disease is graft versus host disease.