Acute Myeloid Leukemia (AML) is a highly aggressive hematologic malignancy characterized by the uncontrolled proliferation of myeloid precursor cells and profound disruption of the immune microenvironment. Among the key contributors to immune evasion in AML are Myeloid-Derived Suppressor Cells (MDSCs), a heterogeneous population of immature myeloid cells with potent immunosuppressive properties. MDSCs play a pivotal role in promoting leukemic progression by inhibiting T-cell activity, fostering regulatory T-cell expansion, and producing immunosuppressive factors such as arginase-1 (ARG1), reactive oxygen species (ROS), and nitric oxide (NO). This review examines the expression, phenotype, and functional roles of MDSCs in AML. Elevated levels of MDSCs have been linked to disease progression, resistance to therapy, and poor clinical outcomes in AML patients. Emerging therapeutic strategies targeting MDSCs hold promise for improving immune responses and treatment efficacy in AML. Furthermore, MDSCs are being investigated as potential biomarkers for risk stratification, treatment monitoring, and prognostication in AML. By synthesizing recent advances, this review underscores the critical role of MDSCs in the pathophysiology of AML and highlights novel therapeutic opportunities aimed at overcoming MDSC-mediated immune suppression.