This model was constructed by introducing the Rpe65 R44X point mutation into the mouse gene by gene editing techniques, resulting in a C to T base substitution at nucleotide 130 of the gene encoding the Rpe65 protein, leading to a stop codon at amino acid position 44 instead of arginine (p.R44*). It has been reported that the eyes of homozygous mice carrying this mutation will not express the RPE65 protein [3]. This model can be used in studies of retinitis pigmentosa 20 (RP20), Leber's congenital amaurosis type 2 (LCA 2), and the visual cycle.