Relevant studies have found that the proportion of CD19 on CD20− B cells is significantly higher in patients with systemic lupus erythematosus and multiple sclerosis and exhibits an activated phenotype.[39,40] This suggests that CD19 on CD20− B cells may produce a large number of autoantibodies through overactivation, which then form immune complexes deposited in myocardial tissues, leading to myocardial damage. The gene discussed is CD19; the disease is systemic lupus erythematosus.