CLCN1 and myotonic dystrophy type 1: We demonstrated that CRISPR-mediated excision of the E7a sequence from the Clcn1 gene was sufficient to restore ClC-1 channel function and eliminate myotonia from the Mbnl1−/− model of DM1 with a resultant decrease in the overt manifestations of myopathy, including and maybe most importantly, significantly improved force production.