Leber congenital amaurosis (LCA) is an untreatable, nefarious, inherited disease that results in children growing up with visual impairment that can range from reduced vision to complete blindness. So far, sixteen genetic abnormalities that lead to the LCA pathology have been identified, with mutations in two of the genes that encode enzymes involved in the visual phototransducation pathway, RPE65 and LRAT, being the culprit behind many cases of LCA (1). In such cases, rods and cones are present, it’s just that the retinal pigment epithelium can’t regenerate the chromophore, 11-cis retinal, so no (or limited) rod or cone signaling occurs. Over time, these cells become dormant, and have been thought to (eventually) die.