The genotyping success rates of all tested SNPs ranged from 95% to 99% and none of the ten SNPs diverged significantly from Hardy-Weinberg equilibrium (P.0.05) ( Table 2 ). The allele and genotype distributions of all tested SNPs in severe sepsis patients, sepsis patients and healthy controls are listed in Table 3 . Our results showed that rs1800629 (2308G/A), located in the promoter region of TNF, was associated with significantly increased risk for severe sepsis. The frequency of rs1800629A in severe sepsis patients was significantly higher than that in both the healthy control subjects (P = 0.00028, OR = 2.08) and the sepsis patients (P = 0.00035, OR = 2.39), and the difference remained significant after Bonferroni correction. Moreover, in multivariate analyses after adjustment for covariates, rs1800629A was still significantly associated with the development of severe sepsis when compared with healthy control group (P adj = 0.00046, ORadj = 1.92) and sepsis group (P adj = 0.002, OR adj = 1.56). The genotype distribution of rs1800629 in the severe sepsis group was also significantly different from that in the healthy control group (P adj = 0.003) and the sepsis group (P adj = 0.004), and the significance remained after Bonferroni correction. However, the difference of the allele and genotype frequencies of rs1800629 between subjects with sepsis and healthy controls were not statistically significant (P.0.05). When we analyzed the allele and genotype distributions of the other nine SNPs (rs361525, rs1799724, rs1799964, rs767455, rs4149570, rs1061622, rs3397, rs1800630 and rs909253), no significant difference was found between the severe sepsis, sepsis and healthy control groups (Table 3) .