As already alluded to earlier, our laboratory and others have shown that PD-1 and its best-known ligand, PD-L1, contribute to the development of shock/ sepsis induced morbidity/ mortality due in part to pathological interactions between myeloid cells, e.g., neutrophils, macrophages, dendritic cells, etc., or non-immune cells, such as vascular endothelial cells [30; 31; 39; 40; 42; 43; 44]. The gene discussed is CD274; the disease is Sepsis.