A combination of blood stasis, plasma hypercoagulability, and endothelial dysfunction is thought to trigger thrombosis.[3] There has been a growing understanding of the central role of inflammation on the local fibrinolytic-thrombotic balance in the initiation of local vascular thrombosis.[6,7] PD-1 pathway inhibitors unleash exhausted T cells in tumors and the reinvigorated T cells evoke inflammation. Here, PDCD1 is linked to endothelial dysfunction.