B2M loss was previously associated with a poor response to ICB treatment45 and is required for an effective CD8+ T cell-mediated anti-tumor immune response.46 However, there are patients lacking B2M that respond to ICB therapy.47 In such instances, reproduced in mice, CD8+ T cells did not efficiently attack the tumor, but the lack of B2M enabled the activation of NK cells and CD4+ T cells that affected tumor growth.47 As we found that CD4+ T cells and NK cells are likely not found in CRATERs in human melanoma, CRATERs indicate a CD8+ T cell-dependent anti-tumor immune response. This evidence concerns the gene B2M and neoplasm.