More recent preclinical developments allow for expression of full-length dystrophins in DMD mouse models (reviewed in Bengtsson et al., 2025), which is achieved by splitting the entire coding sequence over two or three AAVs and using split intein pairs to rejoin the protein products (Tasfaout et al., 2024; Zhou et al., 2024). This evidence concerns the gene DMD and Duchenne muscular dystrophy.