In sepsis, pathogen activation of the immune system leads to a massive release of inflammatory mediators such as cytokines (TNF-α, IL-1β, and IL-6) from immune cells [52], which initiate an autocrine/paracrine cycle leading to excessive cytokine release, which further leads to a cytokine storm production, resulting in a further increase in the inflammatory response and exacerbation of inflammation and injury in the lungs [56]. This evidence concerns the gene IL1B and Sepsis.