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Unlike rapidly reversible modifications, arginine methylation operates through a persistence\u2010prone, forward\u2010biased logic shaped by the lack of a broadly acting demethylase system, multisite substrates, and ongoing methylation flux. Here, we propose a regulatory ratchet framework in which PRMT\u2010dependent methylation can reinforce cellular states through cumulative and network\u2010level effects rather than acting as a binary switch. We integrate PRMT subtype specificity and noncatalytic functions with a four\u2010layer model of substrate selection spanning sequence, structural, localization, and environmental context. Persistence may arise at both mark and flux levels, while scaffold\u2010like PRMT functions may sustain regulatory complexes independently of catalysis. In cancer, PRMT\u2010compatible substrates are distributed across RNA processing, chromatin and transcriptional regulation, signaling, and metabolism, with methylation output shaped by dynamic inter\u2010PRMT relationships. Together, these network\u2010level interactions may reinforce cancer cell states while creating therapeutic vulnerabilities within a constrained methylation system, shifting attention from individual PRMT abundance toward the network architecture that sustains malignant programs.<\/jats:p>","DOI":"10.1002\/1878-0261.70322","type":"journal-article","created":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T11:29:56Z","timestamp":1787657396000},"page":"2466-2489","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Arginine methylation as a regulatory ratchet in cancer: From substrate selection to malignant\u2010state stabilization"],"prefix":"10.1002","volume":"20","author":[{"given":"So Hyun","family":"Kwon","sequence":"first","affiliation":[{"name":"Graduate School of Medical Science and Engineering Korea Advanced Institute of Science and Technology (KAIST)  Daejeon Republic of 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