Deletion of both the exons (45, 46) and (45, 51) or multiple exons (45–51) can restore the reading frame, resulting in the formation of a partially functional dystrophin protein that is associated with a milder form of the disease called Becker muscular dystrophy (BMD) (Fig. 6) [199, 200]. This evidence concerns the gene DMD and Becker muscular dystrophy.