The development of more efficient and safer RNA base editors [138,139,140] as well as more efficient delivery systems targeting diseased cells—such as AAV vectors [138], will realize the use of programmable A-to-I RNA editing using CRISPR-Cas13-fused hyperactive ADAR2 mutant as a future therapeutic strategy for deficient RNA editing-associated neurological diseases, including ALS. This evidence concerns the gene ADARB1 and amyotrophic lateral sclerosis.