<p>Chronic myeloid leukemia (CML) is a malignant clonal proliferative disease originating from hematopoietic stem cells. While treatment with tyrosine kinase inhibitors (TKIs) effectively eliminates the majority of leukemia cells in patients, residual leukemia cells can still be detected in those achieving deep molecular remission, ultimately leading to drug resistance or relapse. But the exact mechanism is unclear. In recent years, the immune microenvironment has been a hot research topic in hematologic malignancies. CML patients exhibit abnormalities in antitumor immunity. Myeloid-derived suppressor cells (MDSCs), which possess immune-suppressing functions, inhibit the proliferation and activation of CD4⁺/CD8⁺ T cells, Tregs, B cells, and NK cells, and play a central role in the antitumor immune response in a wide range of cancers. Abnormalities in numbers and functions of MDSCs are exhibited in CML patients, which affect the immune status of CML patients through multiple mechanisms. This review summarizes the biological properties of MDSCs, their alterations in CML patients, their roles and specific mechanisms in the development of CML, and how these mechanisms can be leveraged to develop new therapeutic strategies, aiming to provide novel insights and approaches for the treatment of CML.</p>