A possible mechanism for Leber's congenital amaurosis has been proposed as the deficiency of RPE65. Without the RPE65 protein, the RPE is unable to store retinyl esters, and the visual cycle is therefore interrupted. At the beginning stages of the disease, the cone cells are unaffected, as they can rely on the alternate Muller cell visual cycle. However, rods do not have access to this alternative and are rendered inert. LCA therefore manifests as nyctalopia (night blindness). In the later stages of the disease, general retinopathy is observed as the rod cells lose their ability to signal. As a result, the rods continually secrete glutamate, a neurotransmitter, at a rate the Muller cells are unable to absorb. The glutamate levels will build up within the retina, where they will reach neurotoxic levels. The RPE65 deficiency would be genetic in origin, and is only one of many proposed possible pathophysiologies of the disease. However, there is a retinal gene therapy to reintroduce normal RPE65 genes that has been approved by the FDA since 2017.