Myocardial fibrosis, assessed by determining CVF, expression levels of a dozen genes involved in fibrosis, and activation of the TGFβ1, was extensive, comprising about 25% of the myocardium, a finding that is in accord with the pro-fibrotic cardiomyopathy caused by the DSP mutations in humans[16,20]. This evidence concerns the gene TGFB1 and Myocardial fibrosis.