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Disease metastasis and relapse in many cancer patients several years (even decades) after surgical remission have been recently acknowledged as cases of cancer dormancy. Although cases of minimal residual disease are well documented, knowledge on its biological mechanisms and clinical implications remains limited. To date, numerous reviews have summarized the three potential models that may explain this phenomenon, including the angiogenic, immunologic, and cellular dormancy. In this study, we discuss newly uncovered mechanisms governing tumor cell dormancy in head and neck cancer, emphasizing on the crosstalk between dormant tumor cells and their microenvironments. Additionally, we explore the mechanisms on the reactivation of dormant residual tumor cells in anatomical sites, including the lymph nodes and bone marrow.