Thus, for example, in vitro TGF-β secreted from astrocytes was shown to curb microglial production of TNF-α and reactive oxygen species [36] whereas evidence from in vivo PD animal models and in vitro astrocyte-microglia cultures indicates that IL-1β, TNF-α, I-CAM1 or ATP released from astrocytes can enhance microglial activation [37, 38]. The gene discussed is TNF; the disease is Parkinson disease.