Dephosphorylation of cMyBP-C has been frequently observed during heart failure (17), likely associated with myocardial β-adrenergic receptor desensitization, and the present results suggest that the depressed force-generating capacity and impaired relaxation are, in part, mediated by dephosphorylated cMyBP-C stabilizing the thick and thin filament OFF and ON states, respectively. Here, MYBPC3 is linked to heart failure.