CTLA4 and neoplasm: The autoimmune reaction against melanocytes in VKH is mainly mediated by T lymphocytes, and the antitumor effects of immune checkpoint inhibitors are also achieved by enhancing T cell function, suggesting that they might be the same T cell clone.21 Interestingly, CTLA4 and PD‐1 genetic polymorphisms have been found among VKH patients.22 CTLA4 and PD‐1 antibodies may disrupt the balance of tumor cell killing and immune tolerance to melanocytes via CTLA4 or PD‐1 signals and therefore be involved in the pathogenesis of VKH.