Correction of other DMD genetic defects, including deletions ΔEx45 [132], ΔEx52 [157], and ΔEx52-53 [158,159] or the duplication of Ex18-30 [160], demonstrated the potential of this CRISPR-based approach to eliminate mutated exon, point mutation, and exonic duplication in different animal models of DMD, notably in large animal such as pigs [161] and dogs [162], paving the way for clinical translation. Here, DMD is linked to Duchenne muscular dystrophy.