Along such lines, polymorphisms in human genes involved in the inflammatory response to infection such as chemokines/cytokines (TNF, IL-6, IL-1 family, macrophage migration inhibitory factor, and IL-10), pattern recognitional molecules (TLRs and Mannose-binding lectin (MBL)), local host defense of the lung (surfactant protein), and coagulation cascades (plasminogen-activator-inhibitor (PAI)-1 and factor V) have been associated with susceptibility to pneumonia and outcomes including sepsis, IPD, and mortality [113–127]. This evidence concerns the gene TNF and pneumonia.