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In addition, there is no dysplasia, nor clinical or molecular criteria for other myeloproliferative neoplasms.<\/jats:p><\/jats:sec><jats:sec><jats:title>Update on Diagnosis<\/jats:title><jats:p>Previously the diagnosis of CNL was often as one of exclusion based on no identifiable cause for physiologic neutrophilia in patients fulfilling the aforementioned criteria. The 2016 WHO classification now recognizes somatic activating mutations of <jats:italic>CSF3R<\/jats:italic> (most commonly <jats:italic>CSF3RT618I<\/jats:italic>) as diagnostic, allowing for an accurate diagnosis for the majority of suspected cases through molecular testing. These mutations are primary driver mutations, accounting for the characteristic clinical phenotype and potential susceptibility to molecularly targeted therapy.<\/jats:p><\/jats:sec><jats:sec><jats:title>Risk Stratification<\/jats:title><jats:p>Concurrent mutations, common to myeloid neoplasms and their precursor states, most frequently in <jats:italic>SETBP1<\/jats:italic> and <jats:italic>ASXL1<\/jats:italic>, are frequent and appear to be of prognostic significance. Although data are evolving on the full genomic profile, the rarity of CNL has delayed complete understanding of its full molecular pathogenesis and individual patient prognosis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ajh.24983","type":"journal-article","created":{"date-parts":[[2018,3,7]],"date-time":"2018-03-07T08:55:10Z","timestamp":1520412910000},"page":"578-587","source":"Crossref","is-referenced-by-count":27,"title":["Chronic neutrophilic leukemia: 2018 update on diagnosis, molecular genetics and management"],"prefix":"10.1002","volume":"93","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7366-9886","authenticated-orcid":false,"given":"Michelle A.","family":"Elliott","sequence":"first","affiliation":[{"name":"Department of Internal Medicine, Division of Hematology Mayo Clinic College of Medicine, 200 First St. SW Rochester Minnesota 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