Virus induction of tumors is the direct effect of a complex interaction of a single virus particle with the target cell. The factor which determines which virus has the potential for inducing tumors resides in the viral nucleic acid and of necessity must be related to the chemical structure of the viral genome. It has been suggested that the important chemical structure is a sequence of bases having a critical degree of commonness with the structure of certain segments of the cell's DNA. The susceptibility of cells to virus transformation might well be universal, but here also there is probably a spectrum of susceptibility dependent upon many structural, physiologic, and karyologic characteristics. However, even the effective entrance of the virus into the cell does not necessarily result in transformation. Replication of the cell DNA may be required for integration of the viral DNA based on homologous areas, and the low efficiency of transformation suggests that this probably requires precise timing of multifactored events. Early stimulation of cell DNA synthesis by induction of increased DNA synthetic enzyme activity may increase the opportunity for integration. Once integration has occurred, virus maturation is suppressed, but derepression of cell DNA synthesis continues. Early viral coded proteins demonstrated as new antigens may play a major role in this derepression. However, fortunately for us, if there is such a thing as tumor viruses of humans, not all virus-transformed cells grow into tumors, since new foreign antigens at the cell surface frequently cause their immunologic rejection.