Studies have shown that lipopolysaccharides (LPS) from gram-negative bacteria or antigens of gram-positive bacteria could induce the production and release of DcR3 in a dose-dependent manner via toll-like receptor 4 (TLR-4) or TLR2 to activate extracellular signal-regulated kinase 1 and 2 (ERK1/2), c-Jun NH2-terminal protein kinase (JNK), and the transcription factor NF-kB [21, 29], which might account for the signal transduction path for the increase of DcR3 with the severity of sepsis. This evidence concerns the gene TNFRSF6B and Sepsis.