DescriptionBreast Cancer (BC) has been a highly prevalent cause of morbidity and mortality in women. The incidence of mortality rate in BC patients increases with age, in which nearly 95% of cases emerge in women over 40 years old. In BC patients, metastasis occurs predominantly in bone marrow (BM) due to interactions between breast cancer cells (BCCs) and resident BM cells. Increasing evidence support a role for the BM as a microenvironmental hub to facilitate breast cancer dormancy and metastasis. Under conditions of dormancy, cancer cells can remain in an undifferentiated state with stem cell-like properties, which confers them with immunological and chemotherapeutic resistance. After initial diagnosis, BCCs can remain dormant for years and even decades before relapsing into metastatic lesions. Epigenetic alterations triggered by resident cells within the BM can be attributed to the initiation and maintenance of BC dormancy. This review focuses on the epigenetic mechanisms underlying BC dormancy within the BM microenvironment, alongside potential therapeutic strategies.