This extends our studies focused on a unique family with DCM with a heterozygous LMNA c.357-2A>G splice-site mutation [37,40,41] by testing the ‘gene expression’ hypothesis that lamin A/C haploinsufficiency may be associated with the dysregulation of epigenomic developmental pathways and the expression of genes with important roles in the nuclear function. This evidence concerns the gene LMNA and familial dilated cardiomyopathy.