Cardiomyocyte-specific expression of a truncated dominant negative CELF protein was shown to specifically disrupt CELF-dependent splicing and leads to the development of cardiac hypertrophy and fibrosis in young (3–9 week-old) mice when expressed in vivo (Ladd et al., 2005a; Ladd et al., 2005b). This evidence concerns the gene CEBPD and cardiac hypertrophy.