Here, we describe the ability of both pro-and anti-inflammatory cytokines, the most represented class of soluble molecules orchestrating inflammatory processes, to enhance the release of MVs from myeloid cells. Additionally, we found this process to be unrelated to that induced by exATP through the activation of its receptor P2X7, but strictly dependent on transcription. Moreover, by using the mouse model of multiple sclerosis, the experimental autoimmune encephalomyelitis (EAE), we found that injection of imipramine, a well-established inhibitor of MV release mediated by exATP (7), did not affect the number of myeloid MVs in the CSF of such mice, with respect to controls. Overall, these findings might suggest the existence of a pathway stimulated by cytokines, but alternative to that centered on the exATP/P2X7 signaling axis, which could be involved in the release of myeloid MVs during inflammatory conditions.