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Dear Editor, Janus kinases (JAKs) are a family of cytoplasmic non-receptor tyrosine kinases (JAK1, JAK2, JAK3, TYK2) associated with cytokine receptors lacking intrinsic kinase activities. Ligand binding to these cytokine receptors activates JAKs, resulting in phosphorylation and homodimerization of signal transducer and activator of transcription (STAT), leading to activation of transcription [1]. JAK1 and JAK3 are associated with the gamma receptor common to receptors of cytokines including interleukins 2, 4, 7, 9, 15, and 21, which play crucial roles in T cell immune responses [1]. JAK2 is associated with the erythropoietin and thrombopoietin receptors [2]. JAK2 gene mutations leading to its constitutive activation are the most common genetic aberration in myeloproliferative neoplasms (MPNs) [2, 3]. Treatment with the JAK 1/2 inhibitor ruxolitinib is highly effective in MPN [3]. However, JAK1 inhibition by ruxolitinib also perturbs the immune response, which is dependent on cytokines and hence JAK/STAT signaling. While these perturbations may be therapeutically exploited, as in treating graft-versus-host-disease [4], they also predispose to infections [5]. People previously infected by hepatitis B virus (HBV) are serologically positive for anti-HBV core antigen antibody (anti-HBc). Subjects who have successfully cleared the virus are negative for HBV surface antigen (HBsAg) and serum HBV DNA. Subjects who still carry the virus are HBsAg-positive. These carriers may in time lose their HBsAg and even serum HBV DNA. However, HBV can still persist as covalently closed circular DNA in the liver, so that viral reactivation and HBV-related complications may occur [6]. Both groups are indistinguishable from each other in routine clinical practice. For practical purposes, subjects anti-HBc-positive, HBsAg-negative, and HBV DNA-negative are considered to have occult HBV infection. With potent B cell depleting immunochemotherapy, viral reactivation might happen in occult HBV infection, with 2-year cumulative rates of 35% in patients with pre-existing anti-HBsAg antibody (anti-HBs) and 68% in those without anti-HBs [7]. In this study, we prospectively evaluated a cohort of MPN patients with occult HBV infection who required treatment with ruxolitinib, in order to define the frequency and time course of viral reactivation. From January 2016 to December 2017, consecutive MPN patients requiring ruxolitinib therapy were studied. Laboratory evaluations included liver biochemistry, serologic tests for anti-HBc, HBsAg, anti-HBs (Abbot Laboratories, Chicago, IL, USA), and serum HBV DNA (Abbott RealTime HBV DNA assay, Abbott Molecular, Des Plaines, IL; lower limit of detection 10 IU/mL); performed before ruxolitinib treatment, then every 4 weeks for the first 3 months and every 3 months thereafter [5]. The primary endpoint was HBV reactivation, defined as detectable serum HBV DNA (≥ 10 IU/mL), irrespective of transaminases or HBsAg status. The secondary outcomes were serum alanine aminotransferase (ALT) level and HBsAg positivity at reactivation. Patients gave informed consent. The study was approved by the Institutional Review Board of the University of Hong Kong and conducted according to the Declaration of Helsinki. In the 2-year study period (data censored at December 31, 2017), 40 Chinese MPN patients required ruxolitinib treatment (Supplemental File 1). Three patients were HBsAgpositive and were given anti-HBV prophylaxis (entecavir, 0.5 mg/day). Of the 37 HBsAg-negative patients, 15 were anti-HBc-positive (Table 1). They all had undetectable serum HBV DNA. None had concomitant chronic liver disease due to other viral hepatitis (C, D), primary biliary cholangitis, Electronic supplementary material The online version of this article (https://doi.org/10.1007/s00277-018-3405-7) contains supplementary material, which is available to authorized users.