FV is a major player in the coagulation cascade. Activated FV is cleaved and degraded by activated protein C, thereby limiting excessive blood clotting. The mutation 1691G>A causes a single amino acid exchange at position 506 (R506Q), which alters a cleavage site and subsequently prevents efficient inactivation of FV. In allele A carriers, persisting FV activity facilitates the generation of other activated coagulation factors and consequently increases the risk of clot formation in veins. Approximately 5% of Caucasians are heterozygous carriers of the FV Leiden mutation. They encounter a 5 to 10 times higher risk of having venous thrombosis, whereas homozygous carriers have a 50 to 100 times higher risk compared to non-carriers. Individuals with additional risk factors, like the presence of other thrombophilic mutations, obesity, hypertension, type 2 diabetes, smoking or intake of oral contraceptives, are even more predisposed to venous thrombotic events.