Mechanistically, autoimmunity has been proposed as a mechanism for the development of post-viral myocarditis, as demonstrated by the presence of antibodies for select antigens, such as cardiac myosin (Myhc), adenine nucleotide translocator (ANT), branched-chain α-ketoacid dehydrogenase kinase (BCKDk) [10], Sarcoplasmic/endoplasmic reticulum Ca2+ adenosine triphosphatase 2a (SERCA2a), β1 adrenergic receptor (β1AR), muscarinic M2 acetylcholine receptor, mitochondrial M7, and cardiac troponin I (cTNI) in DCM patients and CVB3-infected mice [14,15,16]. This evidence concerns the gene TNNI3 and viral myocarditis.