Previous studies have demonstrated that sepsis can induce a spleen-derived population of protective platelets expressing high levels of CD40 ligand (1); platelet MHC class I molecules have been shown to impair CD8+ T cell function during sepsis (11); IFITM3 has been identified as a regulator of fibrinogen uptake and platelet reactivity in non-viral sepsis (16); and glycoprotein VI (GPVI) has been reported to enhance local immune defense in pneumococcal sepsis (17). The gene discussed is CD40LG; the disease is Sepsis.