Early research has confirmed that the tolerance of peripheral B cells is impaired, leading to the production of anti-heart autoantibodies, including autoantibodies against the β1 adrenergic receptor (β1-AR), which mediate cardiomyocyte injury and contractile dysfunction [5] and contribute to the pathogenesis of DCM [6]. The gene discussed is ADRB1; the disease is familial dilated cardiomyopathy.