In a large series of studies in animal experimental models we were able to show that genetic transfer of CIITA into tumor cells of distinct histotype and different H-2 genetic background not only could invariably induce MHC-II gene expression but also could elicit tumor rejection or strong retardation of tumor growth when CIITA-expressing tumor cells were injected into syngeneic immunocompetent hosts [Fig. 5A] [71,72]. Here, CIITA is linked to neoplasm.