Although it has been genetically shown that the RBM20 mutations cause DCM, subsequent cardiac transcriptome analyses and animal models have not yet specified RBM20-regulated genes whose aberrant splicing are critically linked to each of the DCM symptoms such as systolic dysfunction, left ventricle dilatation and a risk of ventricular arrhythmia. This evidence concerns the gene RBM20 and familial dilated cardiomyopathy.