In our 2012 report, we found that the overexpression of Stau1 was able to reverse key splicing defects, for example, the missplicing of exon 11 of INSR and the intronic retention event in the CLC1 pre-mRNA, in the neuromuscular disorder Myotonic Dystrophy Type 1 (DM1). The gene discussed is STAU1; the disease is myotonic dystrophy type 1.