This new gene editing system is based on prime editing, connecting N-terminal mutations in the DMD gene to enable expression of full-length or near-full-length dystrophin. This system also has the advantage of stably incorporating edits into the genome. Current treatments such as exon skipping and microdystrophin gene replacement have not successfully halted disease progression in clinical trials, leaving a critical need for therapies that restore full-length or near-full-length dystrophin, especially for patients with mutations in the N-terminal region of the gene, which have been under-addressed.