A rabbit model, developed by a CRISPR-engineered technique to insert indels into exon 12 and/or 13 leading to a frame-disrupting ANO5 mutation, resulted in ANO5 loss-of-function and resembled the human muscular dystrophy phenotype with dystrophic changes observed in the gastrocnemius, tibialis anterior, tongue, and diaphragm [71]. This evidence concerns the gene ANO5 and muscular dystrophy.