Particularly, missplicing of muscle chloride channel (CLCN1), insulin receptor (INSR), bridging integrator 1 (BIN1) and calcium channel voltage-dependent L type alpha 1S subunit (CACNA1S) results in myotonia, insulin resistance and muscle weakness, respectively, constituting key hallmarks of DM (13,15,36–39). This evidence concerns the gene CACNA1S and Myotonia.