Over the past decade, we have subsequently developed a better DM200 mouse model by making new transgenic mice, breeding them to homozygosity and interbreeding lines, to generate a new DM200 model which expresses mRNAs containing the DMPK 3′UTR with (CUG)200 at a high enough level when induced, to have myotonia, RNA foci and cardiac conduction defects [111]. The gene discussed is DMPK; the disease is Myotonia.