In contrast to PD-L1, the natural killer group 2 member D (NKG2D) ligand Rae-1 binds with NKG2D in T cells or NK cells to activate their tumor-killing activity.132 Shedding, loss of expression, or internalization of ribonucleic acid export 1 (Rae-1) from the tumor cell surface leads to immune evasion, which is associated with poor prognosis in patients with cancer.133–135 Researchers found that GCN5 and PCAF acetylate Rae-1 at K80 and K87 to enhance its stability and protect Rae-1 from shedding to activate the immune surveillance of NK cells and CD8+ T cells. This evidence concerns the gene KLRK1 and neoplasm.