In the context of an ischaemic stroke setting, we have previously shown that AnxA1 (via Fpr2/ALX) is able to act both as a therapeutic and a prophylactic drug, reducing infarct volume and improving stroke outcome in a mouse model of acute experimental stroke [17,29] without increasing the risk of intracerebral haemorrhage [3,29,30]. The gene discussed is FPR2; the disease is stroke disorder.