These impaired mechanisms of thin-filament activation and tension production may contribute to cardiac dysfunction and the associated cardiomyopathies in humans, rats, and mice bearing RBM20 mutations that influence titin splicing (Makarenko et al., 2004; Nagueh et al., 2004; Guo et al., 2012; Methawasin et al., 2014). This evidence concerns the gene RBM20 and cardiomyopathy.