Most induced, as opposed to spontaneous, tumors possess tumor-specific transplantation antigens. Data suggest that the prevalence of these antigens, at least among tumors induced chemically in diffusion chambers, is dependent upon the density of the culture at the time of carcinogen application. Other data show that density inhibition of cell growth is mediated by the interaction of various “growth factors” with their respective cell surface receptors. The juxtaposition of these two observations leads me to hypothesize that the tumor-specific transplantation antigen is an altered growth factor receptor. Development of the hypothesis leads to rational explanations of some paradoxical features of tumor growth in nude mice, to a possible understanding of why spontaneous tumors are nonimmunogenic, and to an explanation of the phenomenon of facilitation of tumor growth by a weak immune reaction.