The host immune system reacts to parasite molecules released during IE rupture (e.g., hemozoin pigment and lipid-associated GPI anchors, so-called “malaria toxins”) through innate immunity receptor signaling (e.g., TLRs) leading to release of pro-inflammatory mediators, namely TNF-alpha, IL-1β, IL-6, and IFN-gamma (48–50). The gene discussed is TNF; the disease is malaria.