The leaking of pro-inflammatory molecules like cytokines, arachidonic acid metabolites, proteins of the contact-phase and coagulation systems, complement factors and acute-phase proteins, as well as hormonal mediators[90] through the compromised BBB into the circulation may generate a systemic immune response syndrome (SIRS)[90,91] characterized by hyper-inflammation or may release anti-inflammatory molecules targeting IL-1β, IL-6 or TNFα resulting in compensatory anti-inflammatory response syndrome (CARS) to block development of SIRS[19]. This evidence concerns the gene TNF and systemic inflammatory response syndrome.