Two well recognized agents found elevated in SIRS and sepsis patients that have been extensively studied by many investigators are tumor necrosis factor (TNF, also called TNF-α) and IL-β [8,9] The injurious effects of TNF on ECs are mediated through TNF receptor (TNFR)-1, one of two different TNF receptors that may be expressed on microvascular ECs in situ [10], and TNFR1 occupancy by ligand results in de novo expression of various pro-inflammatory proteins, such as leukocyte adhesion molecules and chemokines, principally through NF-κB-dependent transcription [11]. Here, TNFRSF1A is linked to systemic inflammatory response syndrome.