The transfer of antitumor immunoreactivity to previously normal, nonimmune lymphoid cells was accomplished by incubating normal C3H mouse spleen cells with RNA extracted from the lymphoid organs of guinea pigs immunized with a chemically‐induced C3H fibrosarcoma. Injections of these cells into normal C3H mice significantly inhibited the development of subsequent isografts of the same tumor. RNA from pigs inmunized with normal C3H tissues was ineffective. RNAase treatment of the RNA preparations removed all activity. Within a completely syngeneic tumor‐host system, strain 2 guinea pig spleen cells were incubated with RNA extracted from the spleens of strain 2 guinea pigs previously immunized with a chemically‐induced strain 2 guinea pig liposarcoma, MCA‐A. Immunoreactivity of these cells was demonstrated by their ability to cause areas of specific immune cytolysis in monolayers of MCA‐A tumor cells in vitro. This reaction was found not to be PHA dependent. Again, treatment of the active RNA preparations with RNAase abolished their efficacy. RNA extracted from the spleens of guinea pigs stimulated nonspecifically by immunization with Freund's adjuvant, but not exposed to the tumor, was ineffective. Incubation of normal lymphoid cells with sol‐ubilized extracts of MCA‐A tumor tissue known to be rich in tumor‐specific transplantation antigens, but not containing RNA, did not reproduce the immune cytolysis produced by the active RNA preparations.