This study introduces a CRISPR-Cas13-based RNA editing system called REPAIR, which enables precise and programmable adenosine-to-inosine (A-to-I) editing in mammalian cells. The system utilizes a catalytically inactive Cas13b ortholog (dCas13b) fused to the adenosine deaminase acting on RNA (ADAR2) domain with a hyperactivating mutation (E488Q), allowing for targeted RNA editing. The system is designed to edit full-length transcripts containing pathogenic mutations without strict sequence constraints. REPAIRv1 was developed, and further engineering led to REPAIRv2, which exhibits significantly higher specificity than previous RNA-editing platforms. The REPAIR system was validated by correcting disease-relevant mutations in mammalian cells, including those associated with X-linked nephrogenic diabetes insipidus and Fanconi anemia. The system was also shown to effectively edit endogenous genes such as PPIB and KRAS. To improve specificity, rational protein engineering was applied to the ADAR2 domain, resulting in REPAIRv2, which has a dramatically reduced number of off-target edits compared to REPAIRv1. The REPAIR system offers several advantages over other nucleic acid-editing tools, including the ability to target any adenosine in the transcriptome without sequence constraints, direct deamination of target adenosine to inosine, and the potential for use in post-mitotic cells such as neurons. Additionally, RNA editing is transient and can be more easily reversed, allowing for temporal control over editing outcomes. The system has potential applications in treating diseases caused by temporary changes in cell state, such as local inflammation, and could be used to modify the function of proteins involved in disease-related signal transduction. The REPAIR system provides a new approach for treating genetic disease or mimicking protective alleles and establishes RNA editing as a useful tool for modifying genetic function. The system has the potential to be further engineered to enable additional RNA editing activities, such as cytidine-to-uridine editing, by fusing dCas13 with other catalytic RNA editing domains. Overall, the REPAIR system represents a promising RNA-editing platform with broad applicability for research, therapeutics, and biotechnology.This study introduces a CRISPR-Cas13-based RNA editing system called REPAIR, which enables precise and programmable adenosine-to-inosine (A-to-I) editing in mammalian cells. The system utilizes a catalytically inactive Cas13b ortholog (dCas13b) fused to the adenosine deaminase acting on RNA (ADAR2) domain with a hyperactivating mutation (E488Q), allowing for targeted RNA editing. The system is designed to edit full-length transcripts containing pathogenic mutations without strict sequence constraints. REPAIRv1 was developed, and further engineering led to REPAIRv2, which exhibits significantly higher specificity than previous RNA-editing platforms. The REPAIR system was validated by correcting disease-relevant mutations in mammalian cells, including those associated with X-linked nephrogenic diabetes insipidus and Fanconi anemia. The system was also shown to effectively edit endogenous genes such as PPIB and KRAS. To improve specificity, rational protein engineering was applied to the ADAR2 domain, resulting in REPAIRv2, which has a dramatically reduced number of off-target edits compared to REPAIRv1. The REPAIR system offers several advantages over other nucleic acid-editing tools, including the ability to target any adenosine in the transcriptome without sequence constraints, direct deamination of target adenosine to inosine, and the potential for use in post-mitotic cells such as neurons. Additionally, RNA editing is transient and can be more easily reversed, allowing for temporal control over editing outcomes. The system has potential applications in treating diseases caused by temporary changes in cell state, such as local inflammation, and could be used to modify the function of proteins involved in disease-related signal transduction. The REPAIR system provides a new approach for treating genetic disease or mimicking protective alleles and establishes RNA editing as a useful tool for modifying genetic function. The system has the potential to be further engineered to enable additional RNA editing activities, such as cytidine-to-uridine editing, by fusing dCas13 with other catalytic RNA editing domains. Overall, the REPAIR system represents a promising RNA-editing platform with broad applicability for research, therapeutics, and biotechnology.