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Mutated MYD88 triggers the expression and activation of HCK that drives multiple pro\u2010survival signaling cascades, including BTK. There are over 40 CXCR4 mutation types in WM. WM patients bearing nonsense CXCR4 variants can present with symptomatic hyperviscosity and show greater resistance to covalent BTK inhibitors (cBTK\u2010i). The cBTK\u2010i zanubrutinib shows greater response activity and\/or improved progression\u2010free survival in WM patients with wild\u2010type MYD88, mutated CXCR4, or altered TP53. New or emerging options for patients progressing on c\u2010BTKi include pirtobrutinib, BGB\u201016673, venetoclax, and sonrotoclax. Combinations of BTK inhibitors with chemoimmunotherapy and BCL2 antagonists have advanced. Algorithms for patients with treatment\u2010na\u00efve and previously treated WM based on genomics, disease characteristics, and co\u2010morbidities are discussed.<\/jats:p>","DOI":"10.1002\/hon.70071","type":"journal-article","created":{"date-parts":[[2025,6,15]],"date-time":"2025-06-15T17:51:51Z","timestamp":1750009911000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Diagnosis and Management of Waldenstrom's Macroglobulinemia"],"prefix":"10.1002","volume":"43","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6393-6154","authenticated-orcid":false,"given":"Steven P.","family":"Treon","sequence":"first","affiliation":[{"name":"Bing Center for Waldenstrom's Macroglobulinemia Dana Farber Cancer Institute  Boston Massachusetts USA"},{"name":"Harvard Medical School  Boston Massachusetts 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