With the knowledge that rodents do not express orthologs of human MIC and that human MICB serves as a functional ligand for mouse NKG2D, we generated a bi-transgenic TRAMP/MICB mouse that recapitulates the onco-immunological characteristics of human MIC+ cancer patients in that: i) MIC is specifically expressed in a given organ and concurrently expressed with oncogenic insults; ii) tumor releases sMIC during disease progression; iii) elevated levels of circulating sMIC correlate with more immune suppressive phenotype and more aggressive diseases [27]. Here, KLRK1 is linked to neoplasm.