Approximately one in nine patients with inherited retinal diseases carries a nonsense mutation—a single genetic typo that prematurely halts protein production, often with devastating consequences. This review examines two revolutionary approaches combating these errors: genome editing tools that rewrite DNA itself, and engineered tRNA molecules that override cellular stop signals. We focus particularly on mutations in the KCNJ13 gene, which cause severe childhood blindness conditions like Leber's Congenital Amaurosis. Recent work by Spillane and colleagues demonstrates that while CRISPR-based editing unexpectedly failed to correct the R166X mutation, engineered tRNA successfully restored potassium channel function—revealing important lessons about biological accessibility and therapeutic design. This analysis suggests that the future of precision medicine may require flexible, multimodal strategies tailored to each mutation's unique context rather than relying on any single technological solution.