The rate of PLB phosphorylation may be the result of a balance between an upregulation in the kinase activity, which has been reported in DCM through phosphorylation, oxidation and O‐GlcNAcylation in diabetic hearts from rodents and human patients57, 58, 59, 60 and changes in phosphatases activity.61, 62. The gene discussed is PLN; the disease is familial dilated cardiomyopathy.