For example, in EBV+ lymphoma patients, the high-affine LMP-1 GGDPHLPTL peptide variant induces the overexpression of HLA-E, which inhibits NKG2A + NK cells and facilitates the spread of EBV-infected tumor cells.104 Similarly, circulating tumor cells (CTCs) in pancreatic cancer upregulate HLA-E through platelet-derived RGS18, thereby evading NK cell-mediated immune surveillance by engaging the HLA-E:CD94-NKG2A immune checkpoint.105 Blocking NKG2A or inhibiting its interaction with HLA-E has become a potential therapeutic strategy. This evidence concerns the gene HLA-E and neoplasm.