Based on this finding, we hypothesize that RBM20 nucleocytoplasmic trafficking and accumulation in sarcoplasmic RBM20 granules underlies the development of RBM20 cardiomyopathy associated with NLS mutations, although disruption of an unknown nonsplicing nuclear function of RBM20 cannot be ruled out at this time. This evidence concerns the gene RBM20 and cardiomyopathy.