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Arginine methylation is a common post-translational modification that exists in three distinct forms-monomethylation, asymmetric dimethylation, and symmetric dimethylation-through which it regulates precursor RNA splicing and maintains cellular homeostasis. Dysregulation of the writing, reading, or erasure of arginine methylation promotes cancer development. Recent studies have identified PRMTs as key regulators of alternative splicing, and aberrant PRMT-driven splicing directly impacts multiple biological processes, including tumor proliferation, apoptosis resistance, metastasis, and immune evasion. This review focuses on the molecular mechanisms by which PRMTs regulate alternative splicing, their connections to oncogenic processes, and the therapeutic implications and challenges of targeting the PRMT-splicing axis in cancer.