Cancer is cause dby genetic changes that activate oncogenes or inactivate tumor supressor genes. The repair orinactication of mutant genes may be effective in the treatment of cancer. Indeed, drugs that target oncogenes can be effective in the treatment of cancer. However, it is still unclear why the inactivation of a single cancer-associated gene would ever result in the elimination of tumor cells. In experimentla transgenic mouse models the consequences of oncogenic inactivation depend upon the genetic and cellular context. In some cases, oncogenic inactivation results in the elimination of all or almost all tumor cells through apoptosis by the phenomenon described as oncogene addiction. In other cases, oncogene inactivation predominanatly results in the terminal differentiation or cellular senescence of tumot cells. In yet others, oncogene inactivation resultsin the apparent loss of the neoplastic properties of tumor cells, which now appear and behave like normal cells; however, upon oncogene reactivation at least some of these celsl rapidly reciver their neoplastic phenotype. Thus, oncogene inactivation can result in a state of tumor dormancy. Hence, understanding when and how oncogene inactivation induces apoptosis, differentiation, and senescence within a tumor will be important when developing effective stratergies fot he treatment of cancer.