In a rat model of autosomal dominant retinitis pigmentosa caused by the P23H mutation within the rhodopsin gene, overexpressing GRP78 alleviates ER stress and preserves photoreceptor function.15 Similarly, GRP78 overexpression reduces nigral dopamine loss and ameliorates behavioral deficits in a rat model of Parkinson's disease induced by elevated human α-synuclein.14 In the present study, we determined whether adeno-associated virus (AAV)2-mediated GRP78 overexpression protects RGC injury in TON and investigated potential mechanisms underlying the effects of GRP78. The gene discussed is HSPA5; the disease is Parkinson disease.