With the shift in mechanistic focus from mis-splicing to RBM20 granules as the causative mechanism in RBM20 cardiomyopathy caused by NLS mutations, an important next step will be to determine whether preventing nucleocytoplasmic trafficking of RBM20 by stabilizing the complex formed between importer proteins and the disrupted core NLS sequence or targeted disassembly of sarcoplasmic RBM20 granules can benefit this disease. The gene discussed is RBM20; the disease is cardiomyopathy.