Namely, we previously reported that: (1) the complement system is fully activated down to the level of the formation of the terminal complement complex; (2) the lectin pathway components are persistently present, up to 5 days post-TBI; and (3) MASP-2 in the brain is significantly increased and associated with TBI severity, indicated by abnormal pupil reactivity and traumatic subarachnoid haemorrhage [23]. The gene discussed is MASP2; the disease is subarachnoid hemorrhage.