In addition, considering the case of recurrent myocarditis in two identical twin young athletes carrying a pathological DSP mutation [22], it has been hypothesized that certain DSP variants determine an increased susceptibility of the cardiac desmosome to mechanical stress, which could determine loss of intercellular connection, unmasking cardiomyocyte epitopes and subsequent formation of self-directed antibodies (anti-heart, anti-intercalated-disc, and anti-desmosome autoantibodies) responsible for the activation and maintenance of autoinflammatory processes. The gene discussed is DSP; the disease is myocarditis.