In addition to β1-receptor-related antibodies, anti-M2 muscarinic receptor (anti-M2) antibodies have been detected in a subset of DCM patients and are closely linked to arrhythmogenesis, possibly by disrupting parasympathetic regulation of cardiac rhythm.[13] Other reported cardiac autoantibodies include anti-myosin and anti-cardiac troponin I (anti-cTnI) antibodies, both of which may directly alter cardiomyocyte ion channel function, promote calcium dysregulation, and contribute to contractile dysfunction. This evidence concerns the gene TNNI3 and familial dilated cardiomyopathy.