TNNI3 and cardiomyopathy: The affected heart showed immunoglobulin G (IgG) deposition on the surface of cardiomyocytes and the mice had high levels of circulating IgG autoantibodies against cardiac troponin I, with no signs of infiltrating immune cells in the myocardium, indicating an inflammatory basis for the cardiomyopathy as well as cardiomyopathy through an altered electrophysiological property of cardiomyocytes (Nishimura et al., 2001; Okazaki et al., 2003).