As both a decrease in MBNL1 and MBNL2 and an increase in CUG-BP1 levels are shown to facilitate retention of embryonic or neonatal splice isoforms in adult organs and reversion of DM1 splice defects in the chloride channel RNA is sufficient to rescue myotonia in mouse models, DM1 is widely recognized as an RNA spliceopathy26, 27, 28, 29, 30, 31, 32, 33. The gene discussed is MBNL2; the disease is myotonic dystrophy type 1.