The pathophysiology of systemic inflammatory response syndrome (SIRS) includes the widespread response by release of pro-inflammatory cytokines such as interleukin 1 beta (IL-1β), interleukin 6 (IL-6), and tumor necrosis factor (TNF), which play a vital role in wound healing with IL-6-associated worse outcomes that can lead to the development of SIRS that has higher mortality rate. This evidence concerns the gene IL6 and systemic inflammatory response syndrome.