Furthermore, to formally demonstrate that the phenotype was due to the expression of mutant rhodopsin, we utilized the helper-dependent adenoviral vector (HDAdV) to replace the mutated rhodopsin gene in the RP patient’s iPSCs with the wild-type rhodopsin gene, thus repairing the gene, and found that the phenotype of the iPSC-derived photoreceptor cells reverted to normal. This evidence concerns the gene RHO and retinitis pigmentosa 1.