We proposed that EBV in its latent state in tumor subtype2 evaded the recognition by CD8 + T cells by downregulating B2M to affect antigen presenting by MHC class I molecules, tumor subtype2 achieved immune escape by continuously expressing LGALS9 to induce functional impairment of T and NK cells, thereby evading recognition and killing by NK cells due to downregulation of MHC class I molecules. This evidence concerns the gene LGALS9 and neoplasm.