HLA-E and neoplasm: For examples, upregulation of CLEC2B and HLA‐E in tumor cells can bind to KLRB1 or CD94/NKG2 on the surface of nature killer cells, TH17 and memory T cells to avert natural killer (NK) cell‐mediated tumor elimination.[35, 36] Expressions of LGALS9, NECTIN1, and poliovirus receptor (PVR) in tumor cells can promote T cells exhaustion by binding to inhibitory receptors of T cells HAVCR2, CD96, and T‐cell immunoreceptor with Ig and ITIM domains (TIGIT), respectively.