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However, the <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> community is faced with several clinical issues that need to be addressed. Ten to 15% of <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> patients are diagnosed in advanced phase, and small numbers of chronic phase (<jats:styled-content style=\"fixed-case\">CP<\/jats:styled-content>) cases experience disease progression each year during treatment. For these patients, <jats:styled-content style=\"fixed-case\">TKI<\/jats:styled-content>s induce only transient responses and alternative treatment strategies are urgently required. Depending on choice of first line <jats:styled-content style=\"fixed-case\">TKI<\/jats:styled-content>, approximately 30% of <jats:styled-content style=\"fixed-case\">CML CP<\/jats:styled-content> cases show suboptimal responses, due to a combination of poor compliance, drug intolerance, and drug resistance, with approximately 50% of <jats:styled-content style=\"fixed-case\">TKI<\/jats:styled-content>\u2010resistance caused by kinase domain mutations and the remainder due to unknown mechanisms. Finally, the chance of successful treatment discontinuation is on the order of only 10\u201320% related to disease persistence. Disease persistence is a poorly understood phenomenon; all <jats:styled-content style=\"fixed-case\">CML<\/jats:styled-content> patients have functional Philadelphia positive (Ph+) stem and progenitor cells in their bone marrows and continue to express <jats:styled-content style=\"fixed-case\">BCR<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">ABL<\/jats:styled-content>1 by <jats:styled-content style=\"fixed-case\">DNA PCR<\/jats:styled-content>, even when in very deep remission and following treatment discontinuation. What controls the maintenance of these persisting cells, whether it is necessary to fully eradicate the malignant clone to achieve cure, and how that might be approached therapeutically are open questions.<\/jats:p>","DOI":"10.1111\/imr.12234","type":"journal-article","created":{"date-parts":[[2014,12,15]],"date-time":"2014-12-15T13:36:30Z","timestamp":1418650590000},"page":"106-123","source":"Crossref","is-referenced-by-count":35,"title":["Do we need more drugs for chronic myeloid leukemia?"],"prefix":"10.1111","volume":"263","author":[{"given":"Tessa L.","family":"Holyoake","sequence":"first","affiliation":[{"name":"Paul O'Gorman Leukaemia Research Centre Institute of Cancer Sciences College of Medical, Veterinary &amp; Life Sciences University of Glasgow Glasgow UK"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"G. 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