RBFOX1 and dilated cardiomyopathy: In mice, this temporal regulation is physiologically important, as Rbfox1 knockdown results in cardiac hypertrophy and splicing defects, which is moreover consistent with the reduction in Rbfox1 expression found in human patients with dilated cardiomyopathy and in hypertrophic heart tissue from mice and zebrafish (Gao et al, 2016).