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Introduction:Ruxolitinib is a JAK inhibitor that was recently approved for treatment of primary and secondary MF and shows impressive symptom control by suppression of inflammation. The observed effects are irrespective of the JAK mutational status. Ruxolitinib is also a promising drug for treatment of acute and chronic GvHD (Spoerl et al., Blood 2014 and Zeiser et al., Leukemia, in press). We recently demonstrated that the immune-modulatory effects of ruxolitinib might at least in part be due to an inhibitory effect on dendritic cell (DC) biology (Heine et al., Blood 2014). Dendritic cells are important antigen-presenting cells, which mature and migrate from the periphery into draining lymph nodes upon antigen contact to prime T cells. This process follows chemokine gradients and requires cytoskeletal rearrangement to allow cell movement along the gradients. Members of the family of small GTPases are critically involved in cell chemotaxis, migration and formation of the immunological synapse allowing DC-T cell interaction. The aim of this study was to define in detail the impact of the JAK inhibitor ruxolitinib on DC migration.