Overall, the recordings of ClC-1 currents and the paired in vivo force-contraction/EMG experiments indicate that the gene-based exclusion of E7a was successful in both recovering ClC-1 channel function to wildtype-levels in Mbnl1−/− mice, and that this was successful in completely eliminating myotonia from these mice, as previously accomplished by splice-switching ASOs8,12. Here, CLCN1 is linked to Myotonia.