To address the discrepancies between these study findings, we used three different syngeneic tumor models, the melanoma B16F10, the prostate tumor TRAMP-C2 (TC2), and the lung carcinoma LLC1, to compare tumor incidence between tumor cells engineered to overexpress the soluble human NKG2D ligand sMICB and the parental tumor cell lines. This evidence concerns the gene KLRK1 and neoplasm.