BALB/c-H-2b (BALB.B) mice are less susceptible to the Friend virus (FV) disease syndrome than congenic BALB/c (H-2d) mice, and spleen cells from FV-infected BALB.B mice are markedly less tumorigenic on transplantation to syngeneic hosts than those from FV-infected BALB/c mice. For these reasons we investigated the expression of FV-associated cell surface antigens on cultured, FV-trnasformed cell lines of BALB.B and BALB/c origin. Both cell lines induced transplantation immunity in syngeneic hosts toward further implantations of the same tumor, BALB.B cells being significantly more potent in this respect than BALB/c cells. BALB.B tumor cells, which produce complete, infectious FV, expressed both the cell surface antigen, FMR (corresponding to the cytotoxic antibodies in anti-FV antisera), and virus envelope antigen (VEA, corresponding to the virus-neutralizing antibodies in the anti-FV antisera). BALB/c tumor cells, on the other hand, which are FV-nonproducers, expressed no FMR antigen, but did express VEA on their surfaces for at least 100 passages in culture. These cells could induce FV-neutralizing but not cytotoxic anti-FMR antibodies when used to immunize syngeneic hosts. The absence of FMR antigen may be the basis for the reduced capacity of BALB/c tumor cells, by comparison with BALB.B tumor cells, to induce transplantation immunity. After about the 125th serial transfer in culture, BALB/c tumor cells spontaneously ceased to express VEA and simultaneously became very weak inducers of transplantation immunity in BALB/c hosts. This loss of VEA did not stem from the loss of either the spleen focus-forming virus or the helper virus genomes from these cells, since both viruses could still be recovered from the cell line.