A prothrombotic metabolite AHR-TF/PAI-1 axis is associated with cancer-associated VTE. In animals with xenografts, an increase in blood levels of prothrombotic metabolites activates AHR signaling within endothelial cells of large veins. AHR activation results in its nuclear translocation and the upregulation of TF and PAI-1 within endothelial cells. Both of these events are known to augment thrombogenesis and inhibit thrombolysis. In concert, this axis may contribute to cancer-associated VTE.