While encouraging, it is unclear whether initial benefits to visual function return would diminish as seen in Leber Congenital Amaurosis (LCA2), a non-mitochondrial disease caused by recessive mutations in the RPE65 gene, where topographical maps of visual sensitivity in retinal regions treated by AAV delivery of the normal RPE65 cDNA had progressive diminution of the areas of improved vision 4–6 years after treatment10. This evidence concerns the gene RPE65 and mitochondrial disease.