RBM20 is the most studied splicing factor in the heart, which has been shown to regulate networks of splicing events, particularly in sarcomere and calcium-handling genes.3–5 Mutations in RBM20 are a frequent cause of familial dilated cardiomyopathy (DCM) which highlights the functional impact of aberrant splicing in the heart.6,7 Loss-of-function studies in mice also uncovered roles for other muscle restricted-splicing factors, namely RBM24 and RBFOX1 in the heart,8,9 but the list of RNA-binding proteins (RBPs) controlling alternative splicing in the heart is far from complete. This evidence concerns the gene RBFOX1 and familial dilated cardiomyopathy.