Given the numerous high-throughput methods to engineer new TALENs,9,10,11 as well as their apparent lack of cytotoxicity,7,10 it should be possible to rapidly extrapolate this NHEJ correction method to other regions of the dystrophin gene as well as other diseases that are caused by a loss of protein function introduced by intragenic insertions, deletions, or aberrant stop codons in non-essential regions, including collagen type VII-associated dystrophic epidermolysis bullosa, Fukuyama congenital muscular dystrophy, and limb-girdle muscular dystrophy type 2B. This evidence concerns the gene DMD and Congenital muscular dystrophy, Fukuyama type.