Retinal diseases tend to effect specific neuron subtypes, ranging from age-related macular degeneration, which is caused by the deterioration of photoreceptors near the central portion of the retina (macula), to glaucoma, which identifies abnormally high intraocular pressure resulting in the death of ganglion cells. Unfortunately, adult mammals are not able to regenerate retinal neurons. Conversely, zebrafish, frogs, and various amphibians are able to completely regenerate their retinal neurons in many different animal models of damage, and restore retinal structure and visual function. The source of regeneration stems from the resident Müller glia cells, which normally provide neuronal support and span all three retinal layers. A critical gene for the initiation of transforming Müller glia into neurons was found to be Ascl1. This led our lab to hypothesize that the introduction and upregulation of Ascl1 in mammalian Müller glia might stimulate them to become retinal neurons after damage, as occurs in these other regenerating species. Indeed, after introducing Ascl1 into the Müller glia of mice, we found newly regenerated retinal interneurons (bipolar cells) that successfully integrated into the retinal circuitry and functionally responded to light stimulus. In addition to Ascl1, we have identified another transcription factor, that when introduced in combination with Ascl1, stimulates the generation of a different retinal interneuron (amacrine cells). Ectopic expression of a proneural transcription factor to stimulate retinal regeneration provides a potential therapeutic intervention for treating blinding diseases, that even now, have few modest treatment options. In contrast to prosthetic devices and stem cell-based therapies, neuronal regeneration via viral injections is advantageous in regards to host tolerance and reducing the invasiveness of a given treatment, since the patient’s own Müller glia are the source cell of the new neurons; and therefore, immunosuppression would likely not be required.