Previous studies have proposed that sequestration of MBNL1 and MBNL2 reduces levels of available MBNL protein, causing the changes of splicing observed in tissue from FECD_REP patients (27,32–33) and in patients with myotonic dystrophy who possess expanded CUG repeats within 3′-untranslated region of the DMPK gene (28–29,34). Here, MBNL1 is linked to myotonic dystrophy.