Analysis of chloride channel (CLCN1) splicing, another gene misspliced in DM1 which has been implicated in chloride channelopathy and myotonia [38,39], revealed no dysregulation in the tibialis anterior (TA) from untreated HSALR mice compared with that from wild-type mice (Figure 6A). This evidence concerns the gene CLCN1 and myotonic dystrophy type 1.