CRX (cone-rod homeobox) is a transcription factor essential for photoreceptor development and maintenance. It binds to the DNA sequence 5'-TAATC[CA]-3' upstream of photoreceptor-specific genes, including opsin genes, and acts synergistically with transcription factors such as NRL, RORB, and RAX to regulate photoreceptor cell-specific gene transcription [UniProt]. Beyond its well-characterized transcriptional role, CRX regulates postmitotic photoreceptor precursor translocation during retinal differentiation in humans 1. Mutations in CRX cause autosomal dominant retinopathies spanning a disease spectrum including Leber congenital amaurosis 7, cone-rod dystrophy 2, and retinitis pigmentosa 2. CRX-associated diseases predominantly result from dominant-negative effects, where mutant CRX interferes with wild-type protein function, though haploinsufficiency also contributes to pathogenesis by compromising photoreceptor precursor differentiation and outer nuclear layer stratification 1. De novo CRX mutations account for approximately 10.34% of de novo mutations in inherited eye diseases 3, while pathogenic CRX variants appear in both East Asian-specific and European populations causing hereditary retinal dystrophies 4. Currently, no curative therapy exists; gene augmentation strategies are being investigated as potential treatments 2.