Tumor dormancy is a critical yet not clearly understood stage of tumor evolution. As an inseparable step of the metastatic cascade, dormancy state has been proposed as a major mechanism of cancer late recurrence and postsurgical relapse. Following the dissemination of tumor cells at secondary sites, these invading cells are again involved with the cancer immunoediting process. Dormant phenotype can be seen in single or clusters of disseminated tumor cells, known as cellular dormancy and tumor mass dormancy, respectively. Generally, tumor cell dormancy is a reversible state of cell cycle arrest known as quiescence. Quiescent phenotype allows dormant disseminated tumor cells to occupy and silently reside and also escape immune and therapeutic assaults in foreign tissues far from their own nurturing microenvironment. Cellular dormancy is a state of biological existence with no detectable clinical trace. Another version of dormancy, tumor mass dormancy, concerns small populations of disseminated tumor cells that reach a state of equilibrium when high rates of cellular proliferation are neutralized with almost equal apoptotic deaths within the cluster. Thus there would be no net growth. Tumor mass dormancy is defined as angiogenic and immune-mediated dormancy, terminated by the angiogenic switch and immune escape, respectively. Various intrinsic and microenvironmental factors regulate tumor dormancy. Among these, immune-mediated mechanisms and immunologic niches of both primary and secondary sites, paradoxically, play a critical role in inducing dormant phenotype and also reawakening dormant seeds as well. The same reason that signifies dormancy also prioritizes it as an undeniable therapeutic target.