In studies involving human aortic endothelial cells, CRP resulted in increased plasminogen activator inhibitor-1 expression and reduction in tPA activity, which may explain the observed relationship between increased inflammation and pro-thrombotic changes in fibrin parameters.31, 32Although diabetes was associated with increased maximum turbidity, there was no clear association between this fibrin parameter and glycaemic control. The gene discussed is CRP; the disease is diabetes mellitus.