Deep venous thrombosis (DVT) is a common disorder that frequently occurs after surgical procedures and trauma and in the presence of cancer or immobilization conditions. However, it can also develop without any of these predisposing factors. This condition directs the researcher's enquiry to investigating the basis of organismal thrombotic predisposition. The common prothrombotic genetic mutations include factor V Leiden, factor II G20210 A, plasminogen activator inhibitor-1, prothrombin A20210, and factor XIII - VIII. Nevertheless, current studies suggest that the thrombotic events are not connected with single gene deletion or homeostatic regulation is also affected by other genetic risk factors. Complex interactions of genetic mutations can be affects different levels of thrombotic system or reinforce each other's effects on homeostatic mechanisms. The analysis of literature, together with the action mechanisms of the classic genetical factors and new suggestions, may contribute significantly to our understanding of the genetic predisposition to venous thrombosis.