Support for this displacement of myomesin comes from the lack of detectable myomesin incorporated into diseased/damaged sarcomeres (Figs 5 & 7) and the high concentration of myomesin 3 protein in the sera of Duchenne muscular dystrophy, Limb-girdle muscular dystrophy and dilated cardiomyopathy patients and animal models [45,60–62,65]. The gene discussed is MYOM3; the disease is Duchenne muscular dystrophy.