FVIIa-released EVs transmit signals from endothelial cells to monocytes. FVIIa, upon binding to EPCR on endothelial cells, activates PAR1. FVIIa-EPCR-PAR1–mediated cell signaling results in the activation of ROCK and upregulation of miR 10a expression. ROCK mediates actomyosin contractility and cytoskeletal reorganization, which results in the shedding of EVs from the plasma membrane. miR 10a is packaged into the FVIIa-released EVs. Monocytes take up FVIIa-released EVs by either membrane fusion or endocytosis, and miR 10a is delivered into the cytosol. TAK1 is the central signaling molecule activated by a vast array of inflammatory stimuli and the crucial player in the activation of NF-κB and subsequently NF-κB–mediated inflammatory gene expression. miR 10a binds to TAK1 and degrades it and thus inhibits NF-κB activation and suppresses inflammatory gene expression. Professional illustration by Somersault18:24.