Deregulation of the alternative splicing of the insulin receptor (INSR), muscle chloride channel (CLCN1), and dystrophin (DMD) mRNAs is associated with the insulin resistance (7, 8), myotonia (9–11), and dystrophic process (12), respectively, while missplicing of amphiphysin 2 (BIN1), ryanodine receptor 1 (RYR1), sarcoplasmic/endoplasmic reticulum Ca2+-ATPase SERCA1 (ATP2A1), and muscle calcium channel CaV1.1 (CACNA1S) may contribute to the skeletal muscle weakness observable in DM1 (13–16). This evidence concerns the gene BIN1 and Duchenne muscular dystrophy.