Summary Meningopneumonitis virus was found to interfere with the development of both the ascitic and solid forms of Krebs 2 carcinoma. The inhibitory action of the virus depended on the concentration of both virus and tumor cells. Complete inhibition was only possible when the virus was administered immediately after the implantation of the tumor. A delay of 1 hour reduced the inhibiting effect of the virus. The anti-tumor action of the virus did not take place in mice immune to the virus nor in mice receiving Aureomycin. The virus did not apparently multiply in the tumor cells, nor was there evidence of destruction of the cells by the virus. The implications of these findings are discussed.