They propose that plasminogen activator inhibitor-1 (PAI-1) is involved in this effect via a ‘PAI-1 cycle’, in which metabolic syndrome upregulates PAI-1 expression to promote angiogenesis, tumour cell migration and procoagulant microparticle formation from endothelial cells, which in turn generate thrombin and further propagate PAI-1 synthesis [47]. The gene discussed is SERPINE1; the disease is metabolic syndrome.