Therefore, gene amplification may abrogate the responses to immunotherapy in patients with mucosal melanoma.32 In addition to GNAQ and GNA11, we found that variants in SF3B1 were common in Japanese uveal melanomas, which could hamper antitumor T-cell responses in the tumor microenvironment.33 Thus, the approval of tebentafusp-tebn in Japan may be beneficial for patients with UM,34 and the development of a strategy to overcome such resistance should be explored in the future. Here, GNA11 is linked to neoplasm.