Therefore, we speculate that the possible immune evasion mechanism in tonsil cancer is that tumor cells produce more soluble NKG2DLs (such as ULBP2/3) to competitively inhibit the high expression of KLRK1, and inadequate expression of ULBP1 cannot produce sufficient soluble ULBP1 for immune evasion (the expression level of ULBP1 is much lower than that of ULBP2/3) (see Fig. 13). Here, ULBP2 is linked to neoplasm.