It has been shown that certain organs are more vulnerable and presage the chain or occurrence of MOD. There is no solid data showing whether the dysfunction will affect single organ or multiple organs. Post-traumatic lung dys- function precedes cardiac dysfunction by 0.6 days, he- patic dysfunction by 4.8 days and renal dysfunction by 5.5 days on average [1,4,5]. This early involvement of the lungs supports the contention of the time dependency and tissue (organ) specificity of SIRS. The mechanism of post-traumatic lung injury and dysfunction occur at least in part through mesenteric lymph-induced activation of neutrophils and activation/injury of endothelial cells. Sub- sequent infiltration of the tissue with activated neutron- phils is time dependent and organ specific [28]. In the shock lung, resuscitation from hemorrhagic shock sec- ondary to trauma increases the myeloperoxidase (MPO) level, an index of neutrophil tissue infiltration, in a near- linear fashion during the first 4 h following resuscitation. However, lung MPO level returned to baseline at 24 h following resuscitation from hemorrhagic shock [28]. This data suggest that a vulnerable window for neutron- phil- mediated lung damage exists during the first 4 h follow- ing resuscitation from hemorrhagic shock in rats [28]. Thus, demonstration of a time-dependency and organ-spe- cificity of the proposed composite biomarkers in a fash- ion similar to SIRS, adds more specificity and sensitivity to the composite biomarkers, which helps the develop- ment of specific intervention before the initiation of the pathogenesis of multi-system organ failure. Figure 3 shows the inflammatory response after trauma in hrs and days