The tumor-specific immunogenicity of most transplanted neoplasms is now well established. It has also been shown that the very animal in which a particular tumor originated can react immunologically to transplants of that tumor [56, 58]. Under these circumstances it is not surprising that the pendulum of opinion has swung from the immunity-is-theoretically-impossible position of the fifties to the currently prevalent belief that neoplasia may actually be the raison d'être for the existence of the homograft type of immune mechanism [40, 111]. It is argued that neoplasia may be largely a vertebrate disease and that this type of immune mechanism evolved to meet this specific threat [15]. Increasingly, the opinion is expressed that were it not for the surveillance function of this mechanism, no vertebrate could long escape death from neoplastic disease [13, 14, 40]. Although this extreme emphasis upon the importance of the immune reaction