CREB1, which requires phosphorylation at Ser-133 for activation and subsequent target gene regulation, has been linked to cardiac dysfunction; overexpression of a dominant-negative CREB mutant in cardiomyocytes led to dilated cardiomyopathy with increased mortality (Fentzke et al., 1998), whereas cardiomyocyte-specific CREB deletion in mice yielded a phenotype similar to WT mice (Matus et al., 2007). This evidence concerns the gene CREB1 and dilated cardiomyopathy.