In this model, B7–H1 expression on various immune cells was upregulated during sepsis; B7–H1 deficiency protected mice from sepsis-induced death, lessened mouse organ damage and lowered inflammatory response; but B7–H1 deficiency showed no effect on changing the bacterial burden though it promotes more macrophages and neutrophils to migrate to the infectious site of peritoneum during sepsis [22]. This evidence concerns the gene CD274 and Sepsis.