Although the pathogenesis of sepsis remains incompletely understood, an excessive pro-inflammatory response has been established as a fundamental component of severe sepsis [14] . The proinflammatory cytokine TNF-a is an essential component in the host immune response to infection and has been widely reported to be an important mediator in severe sepsis and septic shock. High circulating levels of TNF-a were correlated with poor outcomes in sepsis patients [15] . TNF-a and lymphotoxin-a (LT-a) share the same receptors as well as many biological activities, and they are central mediators of immune responses [16] . TNF-a and LT-a are encoded by adjacent gene loci in the central or class III region of the human major histocompatibility complex (MHC), between the HLA class I and II genes on the short arm of chromosome 6 [17] . Several SNPs within the promoter region of TNF (2238, 2308, 2857, 2863, 21031) and the first intron of LTA (+252) were thought to influence TNF-a and LT-a production, and have therefore been identified as candidate variants that might influence susceptibility to and/or outcomes from severe sepsis and infectious diseases [18, 19, 20, 21, 22, 23, 24, 25] . In particular, rs1800629 (TNF 2308) and rs909253 (LTA +252) have been the focus of many investigations on sepsis. Although several studies have identified associations for rs1800629 and rs909253 with sepsis risk or outcomes [18, 19, 20, 23, 24] , other studies have not replicated the associations [21, 26, 27, 28] . This inconsistency may be due to small samples size studied and ethnic differences [29] .