DISCLAIMER: The ideas and opinions expressed in the journal's Just Accepted articles do not necessarily refl ect those of Informa Healthcare (the Publisher), the Editors or the journal. The Publisher does not assume any responsibility for any injury and/or damage to persons or property arising from or related to any use of the material contained in these articles. The reader is advised to check the appropriate medical literature and the product information currently provided by the manufacturer of each drug to be administered to verify the dosages, the method and duration of administration, and contraindications. It is the responsibility of the treating physician or other health care professional, relying on his or her independent experience and knowledge of the patient, to determine drug dosages and the best treatment for the patient. Just Accepted articles have undergone full scientifi c review but none of the additional editorial preparation, such as copyediting, typesetting, and proofreading, as have articles published in the traditional manner. There may, therefore, be errors in Just Accepted articles that will be corrected in the fi nal print and fi nal online version of the article. Any use of the Just Accepted articles is subject to the express understanding that the papers have not yet gone through the full quality control process prior to publication. Abstract Gene expression profi ling studies in the Philadelphia-negative chronic myeloproliferative neoplasms have unraveled signifi cant deregulation of several immune and infl ammation genes that might be of importance for clonal evolution due to defective tumor immune surveillance. Other mechanisms might be downregulation of major histocompatibility (MHC) class I and II genes, which are used by tumor cells to escape antitumor T-cell-mediated immune responses. We have performed whole blood transcriptional profi ling of genes encoding human leukocyte antigen (HLA) class I and II molecules, beta2microglobulin and members of the antigen processing machinery of HLA class I molecules (LMP2, LMP7, TAP1, TAP2 and tapasin). The fi ndings of signifi cant downregulation of several of these genes may likely be of major importance for defective tumor immune surveillance. Since up-regulation of HLA-genes are recorded during treatment with epigenome modulating agents (DNA-hypometylators and DNA-hyperacetylators (histone deacetylase inhibitors)) and interferon-alpha2 our fi ndings call for prospective transcriptional studies of HLA-genes during treatment with these agents.