In favour of the deleterious effects of complement in foetal brain injury, a study showed that C3 is depleted in the blood of neonates who subsequently develop cerebral palsy.31 In addition, complement depletion has shown to improve cerebral blood flow and neurological function after ischaemia in adult rats32 and reduced post ischaemic cerebral infarct volume and atrophy in neonatal rats.33 Other studies showed that complement inhibition failed to prevent brain injury caused by thromboembolic stroke34 and hypoxia–ischaemia35 in adult animals. This evidence concerns the gene C3 and infarction.