In patients with GD, TSHR‐reactive B cells survive deletion and potentially present thyroid autoantigen to T cells inducing proinflammatory cytokines.29 This correlation between the expression of CD32 on monocytes and TRAb titers supported that CD32 played a central role in antibody‐mediated autoimmune disease through antibody‐dependent mechanism. The gene discussed is TSHR; the disease is autoimmune disease.