Light-induced phototransduction cascade in rod and cone photoreceptors is mediated by distinct yet highly homologous proteins. Mutations in genes encoding these proteins, including visual pigments (opsins) and cyclic-nucleotide-gated (CNG) channels, lead to retinitis pigmentosa (RP) or achromatopsia (ACHM), two common hereditary blinding diseases affecting rod and cone photoreceptors, respectively. Recent studies suggest that many phototransduction proteins may be functionally compatible with their homologous counterparts in rods and cones. Based on this, by activating the cone opsin genes in rods of the rhodopsin deficient RP mouse model and the rod specific Cnga1 gene in the cones of the Cnga3 deficient ACHM mouse model, we aim at establishing an innovative treatment approach for these diseases. For this purpose, we will utilize advanced CRISPR/Cas9 technologies along with AAV-mediated gene transfer. Our approach will be tested and optimized in cell culture and in retinal explants and will be finally applied to the respective mouse models. The therapy success on these animals will be assessed on morphological, functional, and behavioral level. In case of success, this study will provide a novel treatment approach for hereditary diseases.