Adult mice grafted i.p. with Ehrlich ascites-carcinoma cells and then exposed to sublethal X—irradiation developed a significantly smaller number of "endogenous" spleen colonies than X-irradiated controls not grafted with tumor cells. Similar results were obtained when bone marrow cells from tumor bearing mice were injected i.v. into lethally X-irradiated mice, so as to produce "exogenous" spleen colonies. In both experiments, the Ehrlich ascites-carcinoma inoculum necessary to reduce significantly the frequency of hemopoietic stem cells was found equal to 8,5x10⁵ cells. This is the number of tumor cells which inhibits the immune reactivity of host mice [1]. These findings are consistent with our working hypothesis that the immunological hyporeactivity of tumor-bearing animals is mediated through a functional defect of primitive bone marrow cells. Such a mechanism of action, similar to that recently proposed by Bennet and Steeves [14] for Friend leukemia virus and by Rowland and Hurd [15] for a chemical carcinogen (dimethylbenzanthracene), may point to a common pathway for the immunosuppression caused by malignant tumors.