One of the putative mechanisms of complement-mediated neuronal death is reflected by the notion that the activation of phosphatidyl-inositol-specific phospholipase C (PI-PLC) after traumatic brain injury [11] renders neurons vulnerable to MAC-mediated lysis by shedding of the glycosyl-phosphatidyl-inositol (GPI)-anchored glycoprotein CD59 from neuronal membranes [2]. The gene discussed is CD59; the disease is injury.