CGP 3466 has been reported to rescue dopaminergic neurons from death and to subsequently inhibit the development of motor symptoms in rodent models of PD by preventing mitochondria-mediated apoptosis.49 Additionally, Bcl-2 overexpression and the deletion of pro-apoptotic BAX and BAK have been shown to exert neuroprotection in ALS mice by blocking the apoptosis of lumbar spinal motor neurons and delaying the onset of symptoms.50 The gene discussed is BAX; the disease is amyotrophic lateral sclerosis.