In a similar case, a gain-of-toxic-function human mutation, S637G, in RBM20 (RNA binding motif protein 20), leads to the mislocalization of this protein in the cytoplasm, the formation of RBM20-ribonucleoprotein granules, and thereby causes severe dilated cardiomyopathy by inhibiting mRNA translation, most likely. This evidence concerns the gene RBM20 and dilated cardiomyopathy.