Other messages bound by both factors whose expression responded to CELF1 induction and whose localization changed in response to Mbnl1 depletion (Results) included Kcnj2, a cardiac inward rectifier potassium channel whose mutation is associated with a syndrome that involves cardiac arrhythmia (Andelfinger et al. 2002), and the sine oculis binding protein homolog Sobp, mutations of which have been linked to intellectual disability (Birk et al. 2010). This evidence concerns the gene MBNL1 and cardiac rhythm disease.