It has been shown previously that substitution of the cMyBP-C serine phosphorylation sites with aspartic acid residues (mimicking activated protein) protects against ischemia-reperfusion injury21, whereas substitution with alanine residues (mimicking deactivated protein) results in cardiac hypertrophy with myofibrillar disarray and fibrosis in mice33. Here, MYBPC3 is linked to cardiac hypertrophy.