Recent scientific evidence has indicated that inflammation plays a fundamental role in all stages of atherosclerosis. Many reports contend that atherosclerosis could represent a chronic phlogistic disorder and its exacerbations could determine acute cardiovascular and cerebrovascular events. C-reactive protein (CRP) is the prototype of the acute phase of inflammation, so it is used as a biochemical marker in the studies demonstrating the relationship between inflammation and atherosclerosis in all its manifestations, both cardiovascular and cerebrovascular (1,3). Few data refer to the relation between the acute phase of inflammation, especially for CRP, and venous thromboembolic disease (VTD). In a prospective study, CRP, fibrinogen, and white blood cell (WBC) count were not associated with risk of venous thromboembolism in healthy subjects during a mean follow-up of about 8 years (4). Moreover, no association between CRP polymorphism/haplotypes and the risk of thromboembolism was observed (5). In another study, CRP did not provide additional information about the diagnosis of deep vein thrombosis and differential diagnosis with inflammatory diseases (6), while in another one it was demonstrated that CRP increases in the first day of admission for deep venous thrombosis (DVT) with a decline in the next days, demonstrating that inflammation could be the result of DVT rather than the cause (7). Steeghs and colleagues conclude that CRP could be used alone or combined with a model of pre-test clinical probability to safely exclude pulmonary embolism (PE) (8). In disagreement with these results, Aujesky and colleagues in a previous study had concluded that CRP cannot safely exclude PE when used alone