For example, mbnl mutants did not exhibit changes in alternative splicing of the zebrafish orthologs of CLCN1, the splicing misregulation of which contributes to myotonia in DM, so the zebrafish may not be an appropriate model for studying myotonia, although it can be used to study many other important disease phenotypes (Lueck et al., 2007a,b). This evidence concerns the gene MBNL1 and Myotonia.