In experiments investigating the radiation response of isogenic mouse lymphoma cells, it was found that significant differences in cell radiosensitivity were detectable when irradiated cells were assayed in sham or 400 R whole-body-irradiated (WBI) animals (3,4). The whole-body dose produces a temporary immune suppression, interfering with any inherent resistance which may be present in the recipients against progressive tumor growth. Further experiments have been carried out with the LSA ascites lymphoma and show that: (a) The TD50 doses (1) for animals challenged with unirradiated cells under the following conditions, unirradiated, 400R WBI, unirradiated + x-ray killed cells, 400R WBI + x-ray killed cells, did not differ at a statistically significant level (3, 4); (b) Pretreatment with x-ray-killed LSA tumor cells for three consecutive weeks prior to challenges by viable cells two weeks later did not alter the TD50 doses for normal controls, killed LSA pretreated recipients (TABLE I), killed spleen-cell treated recipients, and viable AKR lymphoma-pretreated recipients. The TD50 doses were not significantly different under the several conditions noted above; (c) Passive transfer of spleen cells from "immunized" animals (received 3 weekly exposures of killed cells) transferred into animals irradiated with 400 R to suppress nonspecific resistance, and then challenged with viable LSA cells did not show any resistance as measured by TD50 dose in WBI control, Hank's solution-pretreated, killed-spleen-cell pretreated, and killed-LSA-tumor pretreated donors. TD50 doses were not significantly different (TABLE II); (d) However, when 1,500 R irradiated LSA tumor cells were used to challenge unirradiated, WBI, or normal recipients challenged with irradiated cells to which additional x-ray-killed cells were added, differences of TD50 dose were detectable, which were significant at statistically significant levels (Table III). These results indicated that irradiation produced changes in the tumor cells which improved the ability of the recipients to recognize them. Radiationinduced division delay or growth alteration in the surviving cells may permit additional time for the host to mobilize its defenses against the tumor. The nonirradiated tumor onthe other hand would suffer no such disadvantages. Or it may be that tumor cells possess tumor-specific antigens (2) which are not completely exposed. Irradiation may produce sublethal cell injury and cell-surface unfolding, thereby exposing the antigenic sites, or alter the permeability or antigenicity of the cell. No residual heterozygosity was detectable in the strain by transfers of skin, bone marrow, or spleen cells between animals of the same sex. Recessive or deleted antigens cannot be excluded. However, multiple transfers of killed tumor cells, killed spleen cells, or cell extracts to adult animals did not produce any skin-graft detectable alterations of immunogenicity.