MNK1 is a serine/threonine kinase identified as a target for MAP kinase pathways. Using chemical drug, kinase-dead expression or knockdown by RNA interference, we show that inhibition of MNK1 induces the formation of multinucleated cells, which can be rescued by expressing a form of MNK1 that is resistant to RNA interference. We found that the active human form of MNK1 localises to centrosomes, spindle microtubules and the midbody. Time-lapse recording of MNK1-depleted cells displays cytokinesis defects, as daughter cells fuse back together. When MNK1 activity was inhibited, no microtubule defect at the midbody was detected, however, anchorage of the membrane vesicle at the midbody was impaired as lumenal GFP-positive vesicles did not accumulate at the midbody. At the molecular level, we found that centriolin localisation was impaired at the midbody in MNK1-depleted cells. As a consequence, endobrevin – a v-SNARE protein implicated in the abscission step – was not properly localised to the midbody. Altogether, our data show that MNK1 activity is required for abscission.