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Failure of red cell production often results in transfusion dependency with subsequent iron loading requiring iron chelation in lower risk patients. Consistent with previous reports, we have observed haematopoietic improvement in a cohort of patients treated with the oral iron chelator deferasirox (<jats:styled-content style=\"fixed-case\">DFX<\/jats:styled-content>). It has been postulated that <jats:styled-content style=\"fixed-case\">MDS<\/jats:styled-content> patients have a pro\u2010inflammatory bone marrow environment with increased numbers of activated T cells producing elevated levels of tumour necrosis factor (<jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content>), which is detrimental to normal haematopoiesis. We demonstrate that <jats:styled-content style=\"fixed-case\">DFX<\/jats:styled-content> inhibits nuclear factor (<jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>)\u2010\u03baB dependent transcription without affecting its proximal activation, resulting in reduced <jats:styled-content style=\"fixed-case\">TNF<\/jats:styled-content> production from T cells stimulated <jats:italic>in vitro<\/jats:italic>. These results suggest that the haematopoietic improvement observed in <jats:styled-content style=\"fixed-case\">DFX<\/jats:styled-content>\u2010treated patients may reflect an anti\u2010inflammatory effect, mediated through inhibition of the transcription factor <jats:styled-content style=\"fixed-case\">NF<\/jats:styled-content>\u2010\u03baB and support the therapeutic targeting of this pathway, which is aberrantly activated in a large proportion of haematological malignancies.<\/jats:p>","DOI":"10.1111\/bjh.13151","type":"journal-article","created":{"date-parts":[[2014,10,1]],"date-time":"2014-10-01T12:41:42Z","timestamp":1412167302000},"page":"576-582","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":32,"title":["The oral iron chelator deferasirox inhibits <scp>NF<\/scp>\u2010\u03baB mediated gene expression without impacting on proximal activation: implications for myelodysplasia and aplastic anaemia"],"prefix":"10.1111","volume":"168","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4802-3629","authenticated-orcid":false,"given":"Ashish","family":"Banerjee","sequence":"first","affiliation":[{"name":"Centre for Cancer Research MIMR\u2013PHI Institute of Medical Research Clayton Vic. 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