Because the myostatin/AKT/FOXO pathway probably provides a new therapeutic target for cardiomyopathies, and the present findings gained from in vitro transgene expression studies [12], animal models [10,11,13,14,15,16,17] or from studies investigating skeletal muscle atrophy [5,6,9,10], we investigated the expression of molecules of the myostatin/AKT/FOXO pathway and the expression of MAFbx and MuRF1 in cardiomyopathy in humans. The gene discussed is TRIM63; the disease is cardiomyopathy.