Abstract: Tumor metabolic reprogramming and immune escape synergistically promote tumor progression, in which methionine (Met) metabolism plays a key role through epigenetic regulation and immune microenvironment remodelling. This paper systematically summarzes the mechanisms by which aberrant Met metabolism leads to “methionine addiction” and maintains the malignant phenotype of tumor cells, and describes its multiple modulations of the immune system: inducing T-cell depletion, promoting the polarization of M2-type macrophages, inhibiting the activity of NK cells, and enhancing the function of tumor-associated fibroblasts. Furthermore, therapeutic strategies targeting Met metabolism, including methionine-restricted diets, metabolic enzyme (MAT2A, NNMT) inhibitors, and epigenetic targets (PRMT5 inhibitors), are explored to provide theoretical reference for the development of Met-targeted therapies.