Taken together with our recent data (TRPV1 and CNTF expression on astrocytes, and CNTFRα expression on DA neurons) [13], CNTFRα expression on microglia in the SN of both humans with PD and MPP+-lesioned rats suggests that endogenous CNTF derived from TRPV1 activated astrocytes has therapeutic potential to restore motor function in the treatment of PD by inhibiting activated microglia-mediated oxidative stress and/or preventing the progressive degeneration of DA neurons. The gene discussed is CNTF; the disease is Parkinson disease.