Notably, an increased rate of cMyBP-C dephosphorylation, and its subsequent dissociation from the sarcomere and further degradation, has been reported in the heart of animal models and patients with heart failure, myocardial infarction, ischaemia–reperfusion injury and pathological hypertrophy (Baker et al., 2015; Decker et al., 2012; Govindan et al., 2012; Kulikovskaya et al., 2007; Kuster et al., 2014). Here, MYBPC3 is linked to myocardial infarction.