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Dear Sirs, Cerebral vein thrombosis (CVT) is a rare cause of acute stroke and an unusual site of venous thromboembolism (VTE) (1). The pathogenic role of risk factors in such venous thromboses may be different compared with deep-vein thrombosis (DVT) of the lower limbs or pulmonary embolism, the most common manifestations of VTE in clinical practice. Both transient or acquired risk factors (pregnancy/puerperium, oral contraceptives, infection, haematological and autoimmune diseases) and inherited thrombophilia (mainly the prothrombin G20210A polymorphism) are identified as predisposing conditions in patients with CVT (2-5). Increasing data recognise the ABO as a susceptibility locus for VTE, non-O blood group carriers sharing a higher risk of VTE than O blood group carriers (6-13). This association, first described in 1969 in women developing VTE on oral contraceptives (6), was confirmed by subsequent studies, even evaluating ABO genotypes (7-10). Two different systematic reviews of literature and metanalyses, including 21 (11) and 38 studies (12), respectively, consistently reported an approximately twofold increase of risk in non-O blood group carriers compared with O-group subjects. These results were

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