Humans have evolved an intricate haemostatic system designed to maintain blood in a fluid state under physiologic conditions. The blood coagulation system is active, and is poised for explosive generation of thrombin. But, the presence of multiple coagulation inhibitors prevents massive thrombin generation in the absence of a substantial procoagulant stimulus. Inherited thrombophilia is of a multifactorial nature. A point mutation at nucleotide position 1691 of the factor V molecule (factor V Leiden) accounts for the most common cause of inherited thrombophilia. This mutation alters factor V molecule such that it is no longer degraded by activated protein C (APC), yet it still retains its procoagulant activity favouring thrombosis. Also, G20210A mutation of prothrombin gene is a mild risk factor for venous thrombosis. plasminogen activator inhibitor -1 (PAI-1) levels are genetically influenced by a dimorphism characterized by the presence of four or five guanosines (4G/5G) at nucleotide position -675 upstream from the transcription start site in the PAI-1 promoter. However, the evidence regarding the relationship between an elevated PAI-1 plasma level or PAI-1 genetic polymorphism and the risk of venous thromboembolism is conflicting. The present study included 39 cases (15 stroke and 24 DVT patients). Their ages ranged between 20-53 years old. All patients had experienced at least one thrombotic event before the age of 45 years. Twenty healthy normal individuals, age and sex matched, with neither personal nor family history of thrombosis were also included as a control group. Molecular study of factor V Leiden, Prothrombin gene mutation and PAI-1 polymorphism were done using polymerase chain reaction (PCR) for DNA amplification. Also, Protein C, protein S, ATIII, LAC and APC- ratio were performed. The prevalence of the 4G allele of PAI-1 in stroke patients was higher than that in controls with a statistically significant difference was observed. Although the prevalence of the 4G allele of PAI-1 in DVT patients was higher than that in controls, there is no a statistically significant difference was observed. In our study, it can be concluded that carrying the 4G allele of PAI-1 either in heterozygous or homozygous state increases the risk of thrombosis in the presence of other genetic (as FV1691A) or acquired risk factors.